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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
J Perinatol. Author manuscript; available in PMC 2013 November 18.
Published in final edited form as:
PMCID: PMC3832211

Subgaleal hemorrhage in a neonate with factor X deficiency following a non-traumatic cesarean section


This case report describes a term infant born by a non-traumatic, non-instrumented cesarean section that presented with respiratory failure and severe metabolic acidosis secondary to subgaleal hemorrhage (SGH). Further evaluation revealed a functional factor X deficiency that was initially treated with fresh frozen plasma infusions. This report is significant for the occurrence of a SGH in a non-traumatic delivery and emphasizes the importance of obtaining a coagulopathy evaluation in patients with similar presentations. In addition, this case suggests that the mechanism of injury that causes SGH may occur more frequently than previously thought, but does not become clinically significant in patients without an underlying coagulopathy.

Keywords: factor X, subgaleal hemorrhage, subgaleal hematoma neonate, hemophilia and intracranial hematoma, hemophilia and subgaleal hematoma


A subgaleal hemorrhage (SGH) occurs when shearing forces are applied to the scalp during delivery, and large emissary veins in the subgaleal space sever or rupture resulting in the accumulation of blood between the epicranial aponeurosis and the periosteum. The loose connective tissue of the subgaleal space can accommodate up to 260 ml of blood in a typical term infant.1 Symptoms can include respiratory distress, anemia, hypovolemic shock, pallor, hypotension, acidosis and jaundice. SGH is much more common in vacuum and forceps deliveries, but may occur spontaneously, and mortality is reported as high as 12 to 25%.2-5 As blood loss can be massive before hypovolemia is recognized, SGH can be a devastating and potentially fatal result of birth trauma. The risk factors of SGH include macrosomia, prolonged second stage of labor, fetal distress and use of vacuum or forceps with instrument assisted deliveries, contributing to an incidence of 40 to 60/10 000 deliveries.6 The incidence drops markedly to 4:10 000 in spontaneous vaginal deliveries and is rarely reported in non-traumatic cesarean sections. There is literature reporting an association between intracranial hemorrhage and bleeding disorders, but the association between SGH and bleeding disorders is difficult to measure, because reports on this topic are rare and most literature combines SGH and cephalhematoma into a single category of extracranial hemorrhage.7,8 Here we report a case of a term infant born by non-traumatic cesarean section that developed a SGH and was found to have a bleeding disorder associated with a mutation in factor X.


The patient is a 39+1 week gestation male, born to a 30-year-old gravida 2 para 2. Maternal prenatal labs were normal, and maternal medications included only a prenatal vitamin. The delivery was a non-traumatic cesarean section for failure to progress after 2 h of active stage 1 labor. No vacuum or forceps were used. Apgars were 7 at 1 min and 9 at 5 min. Birth weight was 3200 g (40th percentile), length 53 cm (90th percentile) and head circumference 35 cm (50th percentile). The infant received vitamin K and was doing well until 16 h of life, when the physician was called due to an infant temperature of 94.6°F, pallor and increased occipital swelling. Physical exam at that time was significant for a boggy occiput without fluctuation and a soft fontanel.

On admission to the special care nursery, he was noted to be grunting and pale, with a prolonged capillary refill. The capillary blood gas 17.5 h after birth was as follows: pH 7.3, pCO2 18 mm Hg and base deficit −14, with a hematocrit of 20. An umbilical venous catheter was placed. He was intubated and given sodium bicarbonate and a packed red blood cell transfusion. Follow-up gas was pH 6.7, pCo2 46mm Hg and a base deficit −30, at which time he received additional sodium bicarbonate, a normal saline bolus, and was transferred to a level III neonatal intensive care unit at 18 h of life. Following transfer, he received additional packed red blood cells, fresh frozen plasma, sodium bicarbonate, calcium gluconate and a stat head ultrasound. Head ultrasound revealed a SGH. He was also found to have bilateral pneumothoracies requiring a right chest tube. Labs were significant for a coagulopathy (prothrombin time 50.8 partial thromboplastin time 63.6 international normalized ratio (INR) 5.02), which persisted throughout his initial hospital course and required multiple fresh frozen plasma infusions. Family history was negative for bleeding disorders. Hematology was consulted to evaluate, and factor levels were obtained. His factor X level was 4%, indicating a moderate quantitative deficiency in factor X. He was continued on multiple fresh frozen plasma infusions and his coagulopathy improved (Figure 1). He was subsequently transitioned to factor IX complex infusions for long-term therapy. His SGH was shown to be resolving on repeated ultrasounds, and by discharge, his factor X levels were greater than 60% post factor IX complex infusions, with factor 2 levels of 145%.

Figure 1
The response in the international normalized ratio (INR) was followed serially during the first 11 days of life. Arrows indicate when fresh frozen plasma (FFP) was administered.


SGHs can be significant and life threatening, with mortality as high as 25%.2-6 SGH is more common in vacuum and forceps assisted deliveries, although there are reports of SGH in spontaneous vaginal deliveries associated with macrosomia, fetal distress or prolonged second stage of labor.4,6 In the current case, SGH occurred in an infant with a non-traumatic cesarean delivery with no known associated-risk factors. Although SGH is often considered in traumatic or instrumented deliveries, our patient illustrates the important lesson that SGH should also be part of the differential diagnosis in infants with severe acidosis and shock, despite a non-traumatic delivery. In addition, this case demonstrates that SGH in a non-instrumented delivery should prompt an evaluation for bleeding disorders. Although there are rare case reports of SGH in patients with hemophilia, our patient was unique in that his coagulopathy was due to a rare autosomal recessive deficiency in factor X that occurs in 1:1 000 000 people.9,10

As the current patient had no known risk factors for SGH (other than the brief period of failure to progress labor), it is likely that his SGH only became clinically significant due to his bleeding disorder. Traditionally, the mechanism of injury in SGH (i.e. the rupture or shearing of an emissary vein during delivery) was thought to be initiated primarily by vacuum- or forceps-assisted delivery, and typically resulted in devastating extracranial hemorrhage. The current case suggests that the mechanism of SGH may occur more frequently and without inciting factors. In addition, the degree of venous tearing in SGH may be potentially variable such that the smaller tears and subsequent smaller hemorrhages do not become clinically significant in patients without an underlying coagulopathy.


Conflict of interest

The authors declare no conflict of interest.


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