Predictors of severity of subgaleal hemorrhage

During the study period, atotal of 78,589 neonates were born and 6,482 of these births were vacuumassisted deliveries. There were 265 neonates with SGH (3.4 per 1,000 live births) of those 133 were born by vacuum-assisted delivery (20.5 per 1,000 vacuum-assisted deliveries). We excluded data from 57 neonates: 55 had missing data, and 2 were identified as having genetic syndromes. We included data from 208 neonates who met the study criteria. The mean (SD) gestational age (GA) of all the neonates with SGH were 38.7 (1.6) weeks and their birth weight was 3275 (441.9) g.

We identified 119 neonates (57.2%) to be in the SC group. The other neonates (42.8%) were in the NSC group. By univariate analysis, GA, preterm, body length, Apgar score at 1 min, and birth asphyxia of the neonates in the SC group were significantly different from those in the NSC group; however, there were no differences in the maternal obstetric factors or other neonatal characteristics, such as sex, birth weight, and head circumference (Table 1).

Variables with P < 0.2 in the univariate analyses were put into the multivariate regression analysis, except for the GA, body length, Apgar score at 1 min (statistical significance, but no clinical significance), and preterm (no preterm in the NSC group). Finally, antepartum pethidine, vacuum-assisted delivery, duration of the second stage of labor, sex, low birth weight neonate, and birth asphyxia were entered into the multivariate regression analysis (Table 2). By multivariate analysis, neonates in the SC group were more likely to have birth asphyxia (Table 2).

The clinical complications and outcomes are shown in Table 3. By univariate analysis, anemia (odds ratio (OR) = 3.3, 95% CI 1.9-6.0), jaundice (OR = 5.9, 95% CI 3.1-11.2), intensive phototherapy (OR= 31.3, 95% CI 11.6-83.3), length of hospital stay (LOS) >7 days (OR = 32.3, 95% CI 4.33-250), hospital cost, hospital cost >200.00 USD (OR = 11.9, 95% CI 5. 1-27.9), daily hospital cost and daily hospital cost >35.00 USD (OR = 5.3, 95% CI 2.7-10.5) in the SC group were significantly greater than the NSC group (P < 0.001). Two neonates had shock at birth and the maximum onset of shock was 24 h of age. Only one neonate in the SC group died (1/208, 0.5%) on day 7 of life as a result of severe sepsis and septic shock.

The incidence of SGH was 0.6-3.0 per 1,000 live births [4, 9, 10] and 4.6-7.6 per 1,000 vacuum-assisted deliveries [9, 11]. In the present study, there was a high incidence of SGH (3.4 per 1,000 live births) compared with a previous study and especially in vacuum-assisted deliveries (20.5 per 1,000 vacuum-assisted delivery). Prolonged second stage of labor, fetal stress, vacuum-assisted delivery, forceps extraction, macrosomia, maternal nulliparity, placement of vacuum extraction cup over the sagittal suture at a distance too close to the neonate’s anterior fontanel, and failed vacuum extraction were risk factors of SGH [10, 12]. Being preterm and birth asphyxia were the risk factors for serious complications in SGH in the present study. The case fatality rate of SGH was 11.9%−22.8% in previous studies [9, 10, 13, 14], but only one neonate (0.5%) died in the present study despite the higher incidence of SGH.

A dead neonate with SGH who had significant volume loss with anemia, coagulopathy, and shock requiring large volumes of blood and blood product transfusions in a previous study [15] was compatible with the criteria of the SC group in this study. Finally, the risk factors for neonates in the SC group for SGH were being preterm and birth asphyxia compared with the NSC group. No preterm neonate presented in the NSC group. The lower GA had a higher proportion of neonates who received therapy for hypotension [16] because the hemodynamics of the preterm neonates had an afterload/output imbalance. Hypotension in preterm neonates occurs from the combination of poor myocardium contractility, patent ductus arteriosus, and low systemic vascular resistance [17]. Moreover, birth asphyxia may cause myocardial ischemia that presents as impaired myocardial contractility, decreased cardiac output, and tricuspid insufficiency [18]. Perinatal asphyxia in preterm neonates was reported with cardiogenic shock [19]. Preterm neonates (poor cardiac contractility) with birth asphyxia (myocardial ischemia) and SGH (hypovolemic shock) have risks for shock and blood transfusion so the hemodynamics of these neonates should be closely monitored within 24 h of birth and crossmatched with blood products for prompt volume resuscitation. However, there was no statistically significant difference in the Apgar scores at 5 min between the SC and NSC groups.

A strength of this study is that data covering a long period (33 years) were collected. Although there was an increasing trend to perform cesarean section, there was no change in close monitoring and prompt resuscitation in all SGH patients in our unit, and there was a very low mortality rate. Moreover, mostprevious studies mentioned the risk factors for SGH, but very rarely identified the risk factors for SC and cause of death. There are some limitations to this study. It was retrospective with some missing data and records. Neither computerized tomography nor magnetic resonance imaging of the neonates with SGH was performed routinely to evaluate intracranial hemorrhage (ICH) and/or skull fracture. However, the presence of ICH was not correlated with the severity of SGH or mortality, whereas the severity of SGH (severe hypovolemia and coagulopathy) was associated with mortality [15]. Because only one neonate died, we could not identify the risk factors for mortality in the neonates with SGH. Finally, there were no long-term neurodevelopmental outcomes in either group.

Being preterm and birth asphyxia predicted SC in neonates with SGH. Therefore, we should be quick to recognize the signs of SGH and promptly manage neonatal patients to reduce phototherapy requirements, length of hospital stay, and costs.