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Neonatal birth injuries

Neonatal birth injuries
Author:
Tiffany M McKee-Garrett, MD
Section Editor:
William A Phillips, MD
Deputy Editor:
Niloufar Tehrani, MD
Literature review current through: Apr 2025. | This topic last updated: Nov 26, 2024.

INTRODUCTION — 

Birth injury is defined as an impairment of the neonate's body function or structure due to an adverse event that occurred at birth. Injury may occur during labor, delivery, or after delivery, especially in neonates who require resuscitation in the delivery room.

There is a wide spectrum of birth injuries ranging from minor and self-limited problems (eg, laceration or bruising) to severe injuries that may result in significant neonatal morbidity or mortality (ie, intraabdominal or intracranial hemorrhage).

An overview of birth trauma and management of birth injuries will be reviewed here. Additional details regarding specific birth injuries and congenital anomalies are discussed separately:  

Brachial plexus and facial nerve palsy – (See "Neonatal brachial plexus palsy" and "Facial nerve palsy in children".)

Shoulder dystocia – (See "Shoulder dystocia: Intrapartum diagnosis, management, and outcome" and "Shoulder dystocia: Risk factors and planning birth of high-risk pregnancies".)

Subcutaneous fat necrosis – (See "Subcutaneous fat necrosis of the newborn".)

Congenital anomalies – (See "Congenital anomalies: Epidemiology, types, and patterns" and "Congenital anomalies: Approach to evaluation" and "Congenital anomalies: Causes".)

EPIDEMIOLOGY — 

In the United States, the overall incidence of birth injuries ranges from 2 to 3 percent based on an analysis of neonatal discharge records between 2006 and 2014 from the Nationwide Inpatient Sample database [1]. In this study, 80 percent of birth injuries were due to scalp injuries (eg, lacerations and bruising), and the remaining were considered major trauma (eg, clavicular fractures, brachial plexus injuries, and intracranial hemorrhage). During the study period, the risk of scalp injuries increased while major trauma decreased. Major trauma was associated with a greater risk of other complications (eg, hypoxic-ischemic encephalopathy and seizures).

RISK FACTORS

Mode of delivery

Cesarean versus vaginal delivery — Whether cesarean delivery is a protective factor compared with vaginal delivery is uncertain. The relative risks reported with each vary depending on the definition of birth injury used in the study.

In an analysis of the Health Care Cost and Utilization Project Nationwide Inpatient Sample, cesarean delivery was associated with a decreased likelihood of all birth trauma compared with vaginal delivery (adjusted odds ratio [aOR] 0.55, 95% CI 0.53-0.58) [2]. However, when the analysis used the definition of birth trauma developed by the Agency for Healthcare Research and Quality Patient Safety Indicator (AHRQPSI), cesarean delivery was associated with an increased risk of birth trauma (aOR 1.65, 95% CI 1.51-1.81). The AHRQPSI definition did not include clavicle fractures or injuries to the brachial plexus and scalp, which were more frequently seen in vaginal deliveries.

Operative vaginal delivery – Operative vaginal delivery refers to the use of forceps or a vacuum device applied to the fetal head to provide traction and to assist the pregnant individual in delivering the fetus. Forceps and vacuum delivery are each associated with an increase in birth injury compared with nonoperative vaginal delivery (table 1). The sequential use of vacuum extraction and forceps increases the risk over either instrument alone. The neonatal complications of operative vaginal deliveries are discussed in detail separately. (See "Assisted (operative) vaginal birth: Overview", section on 'Neonatal adverse effects and complications'.)    

Fetal factors

Macrosomia – When the fetal weight exceeds 4000 g, the incidence of birth injuries rises as the fetal size increases. In one study, when compared with normosomic neonates, the incidence of birth injury was twofold greater in neonates weighing 4000 to 4499 grams, three times greater in those weighing 4500 to 4999 grams, and 4.5 times greater in those weighing 5000 grams or more [3]. In another study, the incidence of fetal injury was 7.7 percent in neonates with birth weights greater than 4500 grams [4].

The diagnosis of fetal macrosomia and its impact on shoulder dystocia are discussed in greater detail separately. (See "Fetal macrosomia" and "Shoulder dystocia: Risk factors and planning birth of high-risk pregnancies", section on 'Risk factors'.)

Abnormal fetal presentation – The risk of birth injury with vaginal delivery is increased with fetal presentation other than a vertex position, particularly breech presentation. Delivery by cesarean delivery reduces the morbidity associated with vaginal delivery of breech neonates and is discussed separately. (See "Overview of breech presentation" and "Delivery of the singleton fetus in breech presentation".)

Preterm neonates – Preterm neonates are at higher risk for birth-associated fractures, especially multiple fractures, compared with term neonates [5,6]. In a case series of preterm neonates, 71 fractures were reported in 27 neonates (mean gestational age 27 weeks) during admission to a neonatal intensive care unit [6]. Ribs were the most common site of fractures (n = 45).

Maternal factors

Maternal obesity – Maternal obesity (defined as a body mass index greater than 40 kg/m2) is associated with an increased risk of birth injuries. This may be due to the greater use of instrumentation during delivery or the increased risk of delivering a large for gestational age (LGA) neonate, which is associated with an increased risk of shoulder dystocia. [7]. (See "Obesity in pregnancy: Complications and maternal management" and "Cesarean birth: Overview of issues for patients with obesity".)

Other factors – Small maternal stature and the presence of maternal pelvic anomalies are associated with an increased risk of birth injuries. One study reported an increased incidence of birth trauma to the head and neck in male neonates and in neonates born to primiparous mothers [8].

SITE OF CARE — 

Many neonatal birth injuries can be managed in the well-baby nursery. Neonates with significant injuries (eg, intraabdominal or intracranial hemorrhage) resulting in clinical instability (eg, shock) should be monitored in a care setting with full cardiopulmonary monitoring and support. In some cases, consultation with a specialist may be warranted (eg, a neurosurgeon for intracranial hemorrhage or spinal cord injury, an orthopedic surgeon for limb fractures or dislocations). This is discussed in more detail in the sections below.

SUPERFICIAL INJURIES TO THE SKIN AND SOFT TISSUE — 

Soft-tissue injuries are the most common form of traumatic birth injuries and include bruising, petechiae, subcutaneous fat necrosis, and lacerations [9]. Diagnosis is made by physical examination. These injuries are usually self-limiting; however, more extensive injury or signs of clinical instability may prompt further evaluation.

Bruising and petechiae

Clinical features Bruising and petechiae are often seen on the presenting portion of the newborn's body.

Genitalia ‒ Bruising and edema of the genitals are common findings in neonates delivered from the breech position.

Head and neck ‒ Bruising and petechiae of the head and face are often present at birth and seen in neonates who are delivered from the vertex position (especially with a face presentation) or in the setting of a precipitous vaginal delivery. Facial bruising may be quite extensive in neonates who are born with a tight nuchal cord.

Management and outcome

Bruising – This is usually self-limiting. However, significant bruising has been recognized as a risk factor for the development of early and/or severe hyperbilirubinemia. Thus, for neonates with significant bruising, close follow-up after the newborn hospital discharge is recommended to assess for jaundice [10]. (See "Unconjugated hyperbilirubinemia in term and late preterm newborns: Screening".)

Petechiae – Most often, petechiae are present at birth, do not progress, resolve spontaneously, and are not associated with other bleeding. If petechiae are widespread, continue to develop, or if other bleeding is present, a platelet count should be obtained to rule out thrombocytopenia.

Subcutaneous fat necrosis

Clinical features – Subcutaneous fat necrosis (SCFN) is uncommon and usually occurs in the first few weeks of life. It results from ischemia to the adipose tissue, often adjacent to a bony structure, following a traumatic delivery. SCFN is characterized by firm, indurated nodules and plaques on the back, buttocks, thighs, forearms, and cheeks. The nodules and plaques may be erythematous, flesh-colored, or blue (picture 1 and picture 2).

Management and outcome – Typically, this condition is self-limiting, with resolution usually occurring by six to eight weeks of age. These neonates require long-term follow-up to monitor for hypercalcemia, which can develop up to six months after the initial presentation of the skin lesions. (See "Subcutaneous fat necrosis of the newborn".)

Lacerations

Clinical features – Fetal laceration has been reported as the most common birth injury associated with cesarean delivery [11]. In one study of 3108 cesarean deliveries, the fetal laceration rate was approximately 3 percent; 78 percent of the lacerations took place when the cesarean delivery was performed emergently [12]. The lacerations occurred most often on the presenting part of the fetus, typically the scalp and face (eg, ocular area).

Management – The majority of fetal lacerations appear to be mild and require repair with Steri-strips only; however, more severe cases may require plastic surgery for repair [12].

INJURIES TO THE HEAD

Initial evaluation of head injury — Head injuries that occur during delivery can be extracranial (eg, caput succedaneum, cephalohematoma, skull fracture, and subgaleal hemorrhage (figure 1)), or intracranial (subdural, subarachnoid, epidural, intraventricular, and less frequently, intracerebral and intracerebellar) hemorrhages (table 1)).

Evaluation starts with physical examination, including palpation of the head and scalp and monitoring of symptoms (algorithm 1). Neonates who have suggestive physical features (eg, significant edema, hematoma, vital sign abnormalities) and risk factors (eg, forceps or vacuum-assisted delivery, delivery after prolonged pushing during labor) for more severe injury warrant frequent monitoring of vital signs and serial measurements of hemoglobin/hematocrit and their occipitofrontal circumference (OFC). The need for imaging depends on suspicion for intracranial injury, severe cranial injury, or subgaleal hemorrhage, as discussed below.

When to suspect intracranial injury – Intracranial hemorrhage (ICH) should be suspected in neonates with concerning features such as vital sign abnormalities (eg, tachycardia, bradycardia), a bulging fontanelle, apnea, respiratory distress, seizures, hypotonia, or decreased consciousness (algorithm 1). A palpable skull depression and finding of fracture with a depression >1 cm on plain radiographs also suggest the possibility of underlying ICH.

In these cases, we obtain computed tomography (CT) to evaluate for intracranial hemorrhage. CT is generally accepted as the standard modality for diagnosis of ICH, particularly in emergency situations, due to ease of access, shorter scan time, and faster result time [13]. If available, magnetic resonance imaging (MRI) can also be performed for nonurgent diagnosis; however, this modality often requires newborn sedation to achieve good imaging results. Ultrasound can be used to diagnose intraventricular hemorrhage (IVH) but is less useful in the diagnosis of extra-axial hemorrhages (eg, subdural, subarachnoid, and epidural hemorrhages). (See 'Intracranial hemorrhage' below.)

The clinician should have a lower threshold for suspecting ICH in the setting of forceps or vacuum-assisted vaginal delivery or prolonged head engagement during delivery, which have been associated with a higher risk of ICH in some [14-16] but not all [17,18] studies. In one study, the reported incidence of ICH was 16 per 10,000 vacuum-assisted deliveries, 17 per 10,000 forceps-assisted deliveries, and 4 per 10,000 unassisted deliveries [15].

Differentiation of extracranial injuries – In neonates without concern for intracranial hemorrhage, physical features can usually distinguish the type and extent of extracranial injury (algorithm 1). Imaging is usually unnecessary except in cases of diagnostic uncertainty or if more significant injury (eg, depressed skull fracture or subgaleal hemorrhage) is suspected.

Specifically, for neonates with diffuse, potentially fluctuant scalp edema (ie, scalp swelling in a helmet distribution with or without a fluid wave), we obtain a head ultrasound or CT to assess for and confirm the diagnosis of subgaleal hemorrhage (SGH). If an operator who is experienced in neonatal head and scalp ultrasound is available, this is preferable to CT due to the lack of ionizing radiation (image 1). In some institutions, the diagnosis of SGH is made presumptively in those with diffuse scalp edema, and imaging is not universally obtained but is reserved for neonates in whom intracranial hemorrhage or a rapidly expanding SGH is suspected or when there is diagnostic uncertainty (ie, SGH versus cephalohematoma with a large, overlying caput succedaneum). However, if imaging is deferred, it should be performed as soon as there is concern for expansion (eg, rapid increase in occipitofrontal circumference or acute decrease in hemoglobin) before signs of clinical decompensation develop. Early recognition and frequent monitoring are important to survival in these cases [19]. This is discussed in more detail separately. (See 'Subgaleal hemorrhage' below.)

Skull fractures will be identified if CT or MRI was performed for deeper injury. However, if neither was performed, and there is a palpable depression or indentation of the skull with suspicion for head trauma during delivery (particularly if accompanied by extensive ecchymoses over the scalp), we obtain plain radiographs of the skull to evaluate for fracture. If available, ultrasound may be a reasonable alternative. If plain radiographs identify a depressed skull fracture (ie, fracture with skull depression >1 cm), we obtain a CT or MRI to evaluate for associated intracranial hemorrhage. Rarely, skull depression can occur at birth in the absence of trauma or fracture (ie, congenital skull depression) and generally does not require additional evaluation. This is discussed in more detail separately. (See 'Skull fractures' below.)  

Otherwise, swelling over the head is generally caused by cephalohematoma or caput succedaneum. In contrast to caput succedaneum, cephalohematoma does not extend across suture lines. It is not necessary to use imaging to distinguish between these if not obvious on examination. However, in those with apparent cephalohematoma, imaging may be helpful if there is concern that the swelling may represent deeper injury, such as a SGH (eg, because of assisted delivery). In such cases, ultrasound is a useful initial test to characterize the fluid collection; however, it may not clearly depict the location of the hematoma relative to the skull sutures [20]. If necessary, CT or MRI can confirm the subperiosteal location of a cephalohematoma. These findings are discussed in more detail separately. (See 'Caput succedaneum' below and 'Cephalohematoma' below.)

Extracranial injuries

Caput succedaneum — Caput succedaneum is a common extracranial birth injury. It presents at birth after prolonged engagement of the fetal head in the birth canal or after vacuum extraction.

Clinical features and diagnosis – Caput succedaneum is an edematous swelling of the scalp above the periosteum, which is occasionally hemorrhagic (figure 1). Caput succedaneum can extend across the suture lines. It is typically diagnosed on examination and does not require imaging. (See 'Initial evaluation of head injury' above.)  

Management and prognosis Caput succedaneum is generally a benign condition, and it usually resolves within a few days and requires no treatment. Reported complications in neonates with caput succedaneum include:

Necrotic lesions, which can result in long-term scarring and alopecia [21].

Halo scalp ring, which is an annular alopecic ring that occurs in neonates after a prolonged or difficult labor due to compression from the bony prominence of the maternal pelvis [22].

Systemic infection, which may rarely occur as a complication of an infected caput succedaneum [23].

Cephalohematoma — Cephalohematoma is estimated to occur in 1 to 2 percent of all deliveries and is much more common when forceps or vacuum delivery is performed.

Clinical features and diagnosis – Cephalohematoma is caused by a subperiosteal collection of blood caused by rupture of vessels beneath the periosteum (usually over the parietal or occipital bone). Cephalohematoma presents as scalp swelling that does not cross suture lines (figure 1). The swelling may or may not be accompanied by discoloration. Cephalohematomas may not be present at birth and may develop over the first 24 to 48 hours of life. They are often accompanied by caput succedaneum, which can initially obscure the cephalohematoma. Diagnosis is usually made by physical examination and rarely requires imaging. (See 'Initial evaluation of head injury' above.)

Cephalohematomas are also commonly associated with linear, non-depressed skull fractures, which are often unrecognized as the neonate is asymptomatic. (See 'Skull fractures' below.)

Management and prognosis – Cephalohematoma rarely expands after delivery and does not generally cause significant blood loss. The majority of cephalohematomas will resolve spontaneously over the course of a few weeks without any intervention.

Common complications include:

Hyperbilirubinemia – Cephalohematoma has been recognized as a risk factor for the development of early and/or severe hyperbilirubinemia. For all neonates with cephalohematoma, close follow-up after the newborn hospital discharge is recommended to assess for jaundice [10]. (See "Unconjugated hyperbilirubinemia in term and late preterm newborns: Screening".)  

Rarer complications include:

Calcification – Calcification of the hematoma can occur with a subsequent bony swelling that may persist for months. Significant deformities of the skull may occur when calcification or ossification of the cephalohematoma occurs (image 2). Case reports have demonstrated successful surgical excision of these calcified or ossified hematomas [24,25].

Infection – Other complications of cephalohematoma include infection and sepsis. Escherichia coli is the most commonly reported causative agent. Infected cephalohematomas present as erythematous, fluctuant masses that may have expanded from their baseline size. Needle aspiration and culture of the hematoma are required to diagnose infection for suspected cases [26]. Osteomyelitis is a reported complication of an infected cephalohematoma [27]. In these affected neonates, treatment includes incision and drainage of the abscess with debridement of the necrotic skull and a prolonged course of parenteral antibiotics. Details regarding the management of osteomyelitis are discussed separately. (See "Hematogenous osteomyelitis in children: Management".)

Subgaleal hemorrhage — Subgaleal hemorrhage (SGH) has been estimated to occur in 4 of 10,000 spontaneous vaginal deliveries and 59 of 10,000 vacuum-assisted deliveries [28].

Clinical features and diagnosis – SGH develops when blood accumulates in the loose areolar tissue in the space between the periosteum of the skull and the aponeurosis (figure 1). The injury occurs when the emissary veins between the scalp and dural sinuses are sheared or severed as a result of traction on the scalp during delivery.

SGH presents with diffuse, potentially fluctuating scalp edema (ie, scalp swelling in a helmet distribution with or without a fluid wave) and may result in significant anemia or hypovolemia. Early recognition is important, and we obtain imaging for neonates with clinical findings consistent with SGH to confirm the diagnosis. (See 'Initial evaluation of head injury' above.)

Management and prognosis – Neonates suspected of SGH require frequent monitoring of vital signs (minimally every hour) and serial measurements of hemoglobin/hematocrit and their occipitofrontal circumference (OFC). Following diagnosis, measurements should be continued until values are stable or reach normal levels. The OFC increases by 1 cm with each 40 mL of blood deposited into the subgaleal space. Expansion of the swelling due to continued bleeding may occur hours to days after delivery. Affected neonates may have tachycardia and pallor due to blood loss, although blood loss may be massive before signs of hypovolemia and shock become apparent. Neonates should be monitored in a care setting capable of continuous cardiorespiratory monitoring and support due to the potential for rapid clinical deterioration.  

In addition, if SGH is expanding (ie, increasing serial OFC measurements), coagulation studies are warranted to detect coagulopathy that may be associated with the bleeding. Administration of vitamin K at birth should also be confirmed. The clinical manifestations and management of vitamin K-deficient bleeding in newborns are discussed in more detail separately. (See "Overview of vitamin K", section on 'Vitamin K-deficient bleeding in newborns and young infants'.)

Treatment includes volume resuscitation with packed red blood cells, fresh frozen plasma, and normal saline as appropriate for ongoing bleeding and coagulopathy correction. Brain compression requiring surgical evacuation of the hematoma has been reported but is rare [29].

In neonates with SGH, the reported mortality is approximately 12 to 14 percent [30,31] and is due to massive volume loss resulting in shock and coagulopathy [31]. The potential for massive blood loss (50 to 100 mL of blood results in loss of 20 to 40 percent of a neonate's blood volume [32]) is due to the extension of the subgaleal space from the orbital ridges anteriorly, to the nape of the neck posteriorly, and to the level of the ears laterally.

Skull fractures — Birth trauma can result in linear and depressed skull fractures. Depressed skull fractures are often associated with forceps-assisted deliveries. In one report, depressed skull fractures occurred in 3.7 per 100,000 deliveries [33]. Of the 68 depressed skull fractures, 50 occurred with forceps-assisted delivery. The remaining skull fractures were seen in both spontaneous unassisted and elective cesarean delivery, most likely due to pressure upon the soft fetal skull from maternal structures (eg, lumbar vertebrae, sacral promontory, symphysis pubis, and uterine myoma) during labor and delivery.  

Clinical features and diagnosis – Linear skull fractures are usually asymptomatic and may be associated with an overlying cephalohematoma (see 'Cephalohematoma' above). Depressed skull fractures are due to the inward buckling of the skull bones and present with indentation of the skull with or without diffuse ecchymoses over the scalp. The diagnosis of skull fractures is made by imaging. Neonates with a depressed skull fracture should be evaluated for intracranial hemorrhage, a commonly associated finding. (See 'Initial evaluation of head injury' above.)

In rare instances, skull depression is noted at birth in the absence of trauma or fracture. The reported incidence of congenital skull depression is 1 to 2.5 per 10,000 with resolution of the depression occurring over time [34].

Management and prognosis

Linear skull fractures – These typically heal within several weeks and do not warrant follow-up skull radiographs unless the clinician or parent/caregiver prefers them for reassurance.

Leptomeningeal cyst, or growing skull fracture, is a rare, late-presenting complication. This is discussed in more detail separately. (See "Skull fractures in children: Clinical manifestations, diagnosis, and management", section on 'Growing skull fractures'.)  

Depressed skull fractures These are most likely to occur in neonates born via forceps-assisted deliveries and are associated with an increased risk of intracranial bleeding and/or cephalohematoma. Neurosurgical consultation should be obtained in those who have evidence of an intracranial process on imaging, and in those who have a depression greater than 1 cm; these cases often require surgical intervention. The use of a vacuum extractor to elevate significantly depressed fractures has been reported [35].

Smaller fractures (ie, less than 1 cm) without any intracranial injury or isolated congenital skull depression can be managed conservatively with observation only.

Intracranial hemorrhage

Subdural hemorrhage — Subdural hemorrhage (SDH), or hematoma, is the most common type of intracranial hemorrhage noted in neonates, although the overall incidence of clinically relevant SDH is rare. SDH due to birth injury most commonly occurs with vaginal delivery but has also been reported after cesarean delivery [14,16,17,36].

Clinical features and diagnosis ‒ SDH forms between the dura mater and arachnoid membrane (figure 1) [14,17,37]. SDH is most often located in the supra- or infra-tentorial, interhemispheric, or posterior cranial regions [16,18,36].

SDH can be asymptomatic and only identified incidentally [17,38]. Symptomatic neonates usually present within the first 24 to 48 hours of life. Presenting symptoms or findings generally include seizures, respiratory depression, and apnea [13,39]. Other symptoms include signs of neurologic dysfunction such as irritability and altered tone and level of consciousness. Rarely, SDH is associated with increased intracranial pressure resulting in an increase in occipitofrontal circumference (OFC), a tense fontanelle, apnea, bradycardia, and coma. SDH is diagnosed by imaging. (See 'Initial evaluation of head injury' above.)

Management and prognosis ‒ The management and prognosis of SDH depend upon the location and extent of the bleed. Management includes both surgical and medical interventions:

Indication for surgery – Most cases can be managed with conservative therapy without surgical intervention. This is likely due to the plasticity of the neonatal skull, which allows for some degree of expansion without the development of increased intracranial pressure [39].

Surgical evacuation is necessary for neonates with SDH and signs of increased intracranial pressure such as a bulging fontanelle, changes in vital signs and/or pupillary reactiveness, or decreased level of consciousness. SDH that occurs in the posterior fossa, an area of the brain with less skull plasticity, may cause brainstem compression that requires emergent surgical evacuation.

Data on prognosis are limited; however, prognosis is affected by the timeliness of diagnosis and clinical stability at the time of surgical evacuation.

Management of blood loss – Serial hematocrits should be performed in all neonates with SDH to assess for ongoing blood loss. In those with significant blood loss resulting in signs of hypovolemia, normal saline is initially administered for volume replacement, followed by whole blood transfusion. For neonates with an extensive SDH in the absence of overt birth trauma, investigation of a congenital coagulopathy should be considered. (See "Approach to the child with bleeding symptoms".)

Seizure management – Seizure disorders should be treated with antiseizure medication therapy. This is discussed separately. (See "Treatment of neonatal seizures", section on 'First-line ASM therapy'.)

Subarachnoid hemorrhage — Subarachnoid hemorrhage (SAH) is the second most commonly detected neonatal intracranial hemorrhage. SAH can occur with normal, spontaneous vaginal deliveries [13,17] but the risk of SAH increases with operative vaginal deliveries (reported incidences of 2.3 and 3.3 versus 1.3 per 10,000 with vacuum and forceps-assisted deliveries versus spontaneous unassisted deliveries) (table 1) [14].

Clinical features and diagnosis – SAH is most often caused by the rupture of bridging veins in the subarachnoid space or small leptomeningeal vessels. As with subdural hemorrhage, newborns with SAH often present at 24 to 48 hours of life; presenting symptoms include apnea, bradycardia, and seizures [40]. The diagnosis is made by imaging. (See 'Initial evaluation of head injury' above.)

Management and prognosis – Treatment is usually conservative and requires close monitoring of the symptomatic newborn. Most newborns make a full recovery. Rarely, a large SAH can cause posthemorrhagic hydrocephalus.

Epidural hemorrhage — Epidural hemorrhage (EDH) is very rare in neonates. EDH is usually caused by injury to the middle meningeal artery. The rarity of neonatal EDH is attributed to the absence of the middle meningeal artery groove in the neonatal cranial bones, thus making it more difficult to injure the artery. Like the other types of intracranial birth injuries, EDH is often associated with operative deliveries and primiparous mothers [41].

Clinical features and diagnosis – EDH is usually located in the parietotemporal area and is found between the dura and inner table of the skull (figure 1). Neonates with EDH present with nonspecific neurologic symptoms, such as seizures and hypotonia. Increased intracranial pressure may develop and is manifested as a bulging fontanelle, changes in vital signs, and decreased level of consciousness. EDH is often accompanied by a linear skull fracture. EDH and cephalohematoma can coexist when accompanied by an underlying skull fracture due to communication of the bleeding through the skull fracture (figure 1) [42].

Diagnosis is made by imaging which can help to differentiate it from subdural hemorrhage. (See 'Initial evaluation of head injury' above.)

Management – Neonates with very small lesions and a stable clinical course may be managed with supportive therapy. Serial imaging studies (ie, CT or MRI) and close follow up by neurosurgery is required as their condition may rapidly deteriorate due to the arterial source of bleeding. The frequency of imaging depends on the size of lesion and whether there is concern for expansion. Surgical evacuation is necessary when there is evidence of increased intracranial pressure and/or the EDH is large.

In one case series of 15 neonates, surgical treatment was required in 9 neonates with large hematomas (greater than 1 cm thick and 4 cm long), depressed skull fractures, hydrocephalus, and/or shifting of the brain parenchyma [41]. When accompanied by a cephalohematoma, needle aspiration of the cephalohematoma may result in the resolution of the EDH [43].

Intraventricular hemorrhage — Although intraventricular hemorrhage (IVH) is usually associated with preterm delivery, IVH is also reported due to birth injury in term neonates. In a study of 505 healthy asymptomatic term neonates who underwent head ultrasonography within 72 hours of life, the incidence of IVH was 4 percent [44]. All the hemorrhages were subependymal in location (grade 1 IVH). The risk of IVH increases with operative deliveries (reported incidences of 1.5 and 2.6 versus 1.1 per 10,000 for vacuum and forceps-assisted deliveries versus unassisted deliveries (table 1) [14].

The clinical manifestations, diagnosis, and management of IVH are discussed separately. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Clinical features' and "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Management and outcome", section on 'Management'.)

INJURIES TO THE FACE AND NECK

Nasal septal dislocation — Nasal septal dislocation occurs in approximately less than one percent of deliveries due to compression of the nose from the maternal symphysis pubis or sacral promontory during labor and delivery [45]. Neonates with significant trauma can present with respiratory distress due to airway obstruction.

The examination reveals deviation of the nose to one side with asymmetric nares and flattening of the dislocated side. Depression of the tip of the nose can distinguish dislocation from a positional deformity or misshapen nose. With positional deformity, the septum remains straight even though the nares appear uneven. In septal dislocation, application of pressure should cause the nares to collapse, resulting in a more apparent deviated septum, which does not resume a normal position when pressure is released.

Definitive diagnosis is made by rhinoscopy, and referral to an otolaryngologist is needed. Manual reduction by an otolaryngologist using a nasal elevator should be performed by three days of age [45]. No treatment or a delay in treatment may result in nasal septal deformity [45,46].

Ocular injuries

Minor ocular injuries – Minor ocular injuries (eg, retinal and subconjunctival hemorrhages, lid edema) are common and resolve spontaneously without affecting the neonate [47]. Resolution of a retinal hemorrhage occurs within one to five days and a subconjunctival hemorrhage within one to two weeks.

Major ocular injuries – Significant ocular injuries include hyphema (blood in the anterior chamber), vitreous hemorrhage, orbital fracture, lacrimal duct or gland injury, and disruption of Descemet's membrane of the cornea (which can result in astigmatism and amblyopia). They occur in approximately 0.2 percent of deliveries with a higher incidence associated with forceps-assisted delivery [47]. Prompt ophthalmologic consultation should be obtained for neonates with, or who are suspected to have, these injuries.

Facial nerve injury — Facial nerve injury occurs in less than one percent of births and is usually due to compression of the nerve by forceps or a prominent maternal sacral promontory. Typically, only the mandibular branch of the facial nerve is affected resulting in diminished movement on the affected side of the face. Clinical features often include loss of the nasolabial fold, partial closing of the eye, and the inability to contract the lower facial muscles on the affected side, leading to the appearance of a "drooping" mouth. When crying, the mouth is drawn over to the unaffected side.

Facial nerve palsy due to birth trauma should be differentiated from those due to developmental, syndromic, or other etiologies (eg, congenital unilateral lower lip palsy, also referred to as asymmetric crying facies). Traumatic facial nerve palsy has an excellent outcome with spontaneous resolution usually within the first two weeks of life but can be associated with brachial plexus palsy in a small number of cases [48]. The evaluation and management of facial nerve and brachial plexus palsy are discussed separately. (See "Facial nerve palsy in children" and "Neonatal brachial plexus palsy".)  

Laryngeal nerve injury — Laryngeal nerve injury during birth may cause vocal cord paralysis. Symptoms include stridor, respiratory distress, hoarse, faint or absent cry, dysphagia, and aspiration.

The diagnosis is made by direct laryngoscopy. Treatment is dependent upon the severity of the injury. Paralysis will usually resolve over time. (See "Common causes of hoarseness in children", section on 'Vocal fold paralysis'.)

INJURIES TO THE SPINAL CORD — 

Spinal cord injuries include spinal epidural hematoma, vertebral artery injuries, traumatic cervical hematomyelia, spinal artery occlusion, and transection of the cord. They are uncommon with an incidence of 0.14 per 10,000 live births [49]. Risk factors include forceps-assisted delivery and breech vaginal delivery [49].

Clinical features – Spinal cord injuries occur more frequently in the upper cervical spine because of the greater likelihood of injury due to traction or rotation of that area of the cord during delivery.

Clinical findings depend on the severity and spinal level of the injury and include neurological and other abnormalities that localize to the level at or below the injury. For example, high cervical or brainstem lesions may present with respiratory distress or paralysis and abnormal reflexes of the upper extremities. Lower spinal cord lesions may present with paralysis, hypotonia, and abnormal reflexes of the lower extremities.

Diagnosis – The diagnosis is often initially made by ultrasonography. If available, MRI provides better visualization of the spinal cord and is the preferred modality. Brachial plexus injury is an associated finding in neonates with cervical spine subluxation or spinal cord injury, and an examination should be performed to evaluate for this injury (table 2). Neonatal brachial plexus palsy is discussed in greater detail separately. (See "Neonatal brachial plexus palsy".)

Management and prognosis – Management can be surgical or non-surgical (eg, use of orthotics) and requires consultation with a clinician who specializes in cervical spine trauma (eg, neurosurgeon or orthopedic surgeon) [50,51]. Severe high cervical or brainstem lesions have a high mortality rate [49]. Lower lesions may result in significant morbidity with permanent neurologic impairment.

INJURIES TO THE ABDOMEN — 

Intraabdominal injury primarily consists of rupture or subcapsular hemorrhage into the liver, spleen, and adrenal gland [52]. Intraabdominal birth trauma is uncommon. Macrosomia, breech delivery, and the use of instrumentation during delivery have been reported as risk factors for abdominal birth injuries [53].

Clinical features – Clinical findings depend upon the amount of blood loss. Neonates with hepatic and splenic rupture may present with sudden pallor, signs of hemorrhagic shock, and abdominal distension and discoloration, whereas those with subcapsular hematoma may have a delayed or more insidious onset of symptoms of anemia such as poor feeding, tachycardia, and tachypnea. Unilateral adrenal hemorrhage may present as an abdominal mass. The physical examination of the abdomen in neonates is discussed separately. (See "Assessment of the newborn infant", section on 'Abdomen'.)

Diagnosis – Ultrasonography is the best modality to diagnose intraabdominal birth injuries and can be performed at the bedside. CT can also provide useful diagnostic information, but transport of a critically ill neonate to the scanner is more difficult.

Management and prognosis – The management includes fluid resuscitation with blood products and normal saline as appropriate. Fresh frozen plasma may be needed to correct any coagulopathy associated with the injury. In neonates with hepatic or splenic rupture or who are hemodynamically unstable, laparotomy may be warranted to control the bleeding [52]. The management of neonatal shock is discussed separately. (See "Neonatal shock: Management".)

Prognosis depends on the severity of injury and the complications resulting from it. Prompt diagnosis and management lead to better outcomes.

INJURIES TO THE LIMBS

Initial evaluation of limb injury — Injuries of the limbs may affect both upper and lower extremities and include nerve injuries, fractures, and dislocations. Evaluation begins with physical examination. Significant limb injury should be suspected in neonates with abnormal positioning of the extremities and asymmetric or decreased neonatal reflexes or movement of the extremities. More rapid presentation of symptoms, or associated symptoms such as respiratory distress, asymmetric bone contour, crepitation, or increased pain response (eg, crying) with movement, may indicate more severe injury, although some fractures can present without symptoms. Clinicians should have a higher suspicion for injury in neonates with difficult vaginal delivery, breech presentation, shoulder dystocia, or fetal macrosomia, particularly if abnormalities are detected during delivery. (See "Assessment of the newborn infant", section on 'Extremities' and "Neurologic examination of the newborn", section on 'Reflexes'.)

When limb injury is suspected, we typically perform plain radiographs of the affected area:

When abnormalities localize to the upper extremities, we obtain radiographs of the bilateral clavicles, the chest, and/or the affected arm to distinguish between clavicular fractures, traumatic separation of the proximal humeral epiphysis, humeral shaft fractures, or shoulder dislocations [54]. Plain radiographs to assess multiple areas (eg, bilateral clavicles and humeri) may be warranted if the neonate is at higher risk for multiple fractures (eg, shoulder dystocia, difficult extraction during delivery). (See 'Clavicular fractures' below and 'Humeral fractures' below and 'Dislocations' below.)

When abnormalities localize to the lower extremities, we obtain radiographs of the pelvis (which provides bilateral views) and legs (eg, to diagnose proximal femoral fractures). (See 'Femoral fractures' below and 'Dislocations' below.)

Plain radiographs may not detect epiphyseal fractures (Salter-Harris Type I fracture) or differentiate dislocations from these types of injuries due to the lack of ossification of the epiphysis in neonates [55,56]. In these cases, ultrasonography or MRI can help to detect the injury [57,58]. While MRI may be a less painful modality than ultrasound, it is more expensive and may be less readily available.  

The neonate should be evaluated for associated nerve injury if a clavicular, humeral fracture, or shoulder dislocation is found, or if plain radiographs are normal but other physical findings are present (table 2). (See "Neonatal brachial plexus palsy", section on 'Evaluation and diagnosis' and "Diaphragmatic paralysis in the newborn", section on 'Clinical features'.)

The clinical manifestations and management of specific types of limb injuries at birth are discussed below. Epiphyseal plate separations and fracture management in children are discussed separately. (See "General principles of fracture management: Fracture patterns and description in children".)

Fractures

Clavicular fractures — Clavicular fractures are the most commonly reported fractures in neonates. The incidence of clavicle fractures due to birth trauma ranges from 0.5 to 1.6 percent [59-61]. Fractured clavicles are often associated with difficult vaginal delivery; however, clavicular fractures also occur in neonates born via normal spontaneous vaginal or cesarean delivery. Reported risk factors for clavicular fractures include operative delivery, shoulder dystocia, increased maternal age, increased birth weight (particularly if >4 kg), and lower mean head-to-abdominal circumference ratio [59-61].

Clinical features and diagnosis ‒ The timing of the presentation is dependent on whether the fracture is displaced or nondisplaced:

Displaced (complete) clavicle fractures are more likely to be accompanied by physical findings in the immediate post-delivery period. These include crepitus, edema, lack of movement of the affected extremity, asymmetrical bone contour, and crying with passive motion.

Nondisplaced clavicular fractures are usually asymptomatic. Diagnosis is often delayed by days or weeks until there is a formation of a visible or palpable callous.

The diagnosis is made by plain radiographs (image 3). All neonates with clavicular fractures should also be evaluated for brachial plexus palsy, a commonly associated injury (table 2). (See 'Initial evaluation of limb injury' above.)

Rarely, congenital pseudarthrosis of the clavicle may present on radiographs as an asymptomatic incidental finding [62]. No acute treatment is typically needed; however, the patient should be referred to an orthopedic specialist for evaluation and management.  

Management and prognosis Clavicular fractures in neonates heal spontaneously within two to three weeks with no long-term sequelae [63]. Thus, parental reassurance and gentle handling are all that are required for management. We prefer using comfort measures over analgesics for pain control to avoid masking concerning symptoms, (eg, fever or substance withdrawal) in the neonate. For comfort, the arm on the affected side can be placed in a long-sleeved garment and pinned to the chest with the elbow at 90 degrees of flexion. Signs of healing on physical examination (such as resumption of spontaneous arm movement and lack of tenderness at the fracture site) and callus formation seen on plain radiographs are usually predictive of appropriate healing. Repeat imaging is usually not necessary. If there is concern for abnormal healing, a repeat plain radiograph at a few weeks of age can help determine whether there is proper remodeling of the bone.

Humeral fractures — Although it is the most common long bone fracture in neonates, humeral fractures are rare with a reported incidence of 0.2 per 1000 deliveries [64]. Risk factors for humeral fractures include shoulder dystocia, macrosomia, cesarean delivery, breech delivery, and low birth weight [65-67].

Clinical features and diagnosis ‒ Most fractures occur at the proximal third of the humerus and are transverse and complete [65]. Clinical manifestations include decreased movement of the affected arm, decreased Moro reflex, localized swelling and crepitation, and an increased pain response with palpation and movement of the arm.

The diagnosis is made by plain radiographs of the arm (image 4 and image 5). Brachial plexus injury is a commonly associated finding in neonates with humeral fractures, and examination should be performed to evaluate for this injury (table 2). (See 'Initial evaluation of limb injury' above.)

Management and prognosis ‒ Treatment of humeral fractures consists of immobilization of the affected arm with the elbow in 90-degree flexion to prevent rotational deformities [68]. The humerus can be stabilized against the thorax by an elastic wrap or long-sleeved shirt.

Prognosis is excellent, and parents should be reassured that bone deformity will resolve due to remodeling as the neonate grows. Signs of fracture healing on physical examination include regaining of spontaneous arm movement. Repeat imaging is not necessary if physical examination is reassuring. If there are clinical or parent/caregiver concerns, plain radiographs to confirm healing can be performed at three to four weeks post-injury, although evidence of callus formation is often seen on radiography by seven to ten days.

Femoral fractures — Fractures of the femur as a result of birth trauma are rare, with a reported incidence of 0.13 per 1000 live births [5]. In a large series of 55,296 live births, risk factors for femoral fractures included twin pregnancies, breech presentations, prematurity, and diffuse osteoporosis [5]. Differential diagnosis includes metabolic bone disorders and nonaccidental trauma.

Clinical features and diagnosis ‒ The fracture is typically spiral and involves the proximal half of the femur. Neonates with femoral fractures may be asymptomatic and only identified incidentally. Symptoms can also be subtle, with only an increased pain response upon manipulation of the affected extremity. In some cases, swelling of the affected leg may be present. A "pop" or "snap" may be noted upon delivery of the legs during vaginal breech extraction and should prompt investigation.

The diagnosis is made by a plain radiograph of the leg. (See 'Initial evaluation of limb injury' above.)

Management and prognosis ‒ The Pavlik harness is generally used to treat neonatal femoral fractures [69]. The fracture is reduced by adjustment of the harness straps. Consultation with a pediatric orthopedic surgeon is warranted. Care needs to be taken when applying this device as a poorly fitting Pavlik harness can lead to femoral nerve palsies and avascular necrosis of the hip. A more complete discussion on the use of the Pavlik harness is found separately. (See "Developmental dysplasia of the hip: Treatment and outcome", section on 'Pavlik harness'.)

Prognosis is excellent, and evidence of callus formation is usually seen on radiography by seven to ten days, but this is not routinely necessary. If there are concerns, radiographs can be performed at three to four weeks postinjury to confirm healing. Nonanatomic alignment is common and acceptable, and parents/caregivers should be reassured that bone deformity will resolve via remodeling as the neonate grows.

Nerve injuries — Nerve injuries at birth include brachial plexus and phrenic nerve injuries.

Brachial plexus injury or palsy is one of the most common neurologic birth injuries. Clinical manifestations vary depending on the pattern of nerve involvement (table 2). The diagnosis and management of this injury are discussed in greater detail separately. (See "Neonatal brachial plexus palsy".)

Phrenic nerve injury is often associated with brachial plexus injury. Clinical manifestations include respiratory distress with diminished breath sounds on the affected side due to diaphragmatic paralysis. Symptoms typically present on the first day of life. The diagnosis and management of neonatal diaphragmatic paralysis are discussed separately. (See "Diaphragmatic paralysis in the newborn".)  

Dislocations — Dislocations caused by birth trauma are extremely rare. In most cases, the dislocations, especially of the hip and knee, are due to intrauterine positional deformities or congenital malformations. Early referral to orthopedic surgery is warranted.  

Clinical features and diagnosis – Diagnosis is made by physical examination and imaging studies (picture 3). Shoulder subluxation/dislocation can be associated with brachial plexus palsy and neonates should be evaluated for this injury [70]. (See 'Initial evaluation of limb injury' above.)

Management and prognosis – Management and prognosis vary depending on the type of injury:

Shoulder dislocation – If the neonate has a shoulder dislocation, more urgent intervention and referral to orthopedic surgery are required [71]. Treatment typically includes splinting and conservative management with early referral to physical and occupational therapy to maintain passive motion. In some cases, surgical correction may be required and becomes an option when the neonate is older.

Hip dislocation – Early orthopedic referral is necessary for effective management. In some cases (eg, teratologic hip dislocations in arthrogryposis or myelomeningocele), reduction may not be necessary. In general, management is similar to patients with dislocation due to congenital hip dysplasia. This is discussed in more detail separately. (See "Developmental dysplasia of the hip: Treatment and outcome", section on 'Age 0 to 4 weeks'.)

Knee dislocation – This is rare and may occur in isolation or be associated with a syndrome such as arthrogryposis multiplex congenita. We refer to orthopedic surgery during the newborn hospitalization. Treatment consists of serial casting and/or surgical correction.

SUMMARY AND RECOMMENDATIONS

Incidence ‒ In the United States, the overall incidence of birth injuries ranges from 2 to 3 percent. The most common type is scalp injuries (eg, lacerations and bruising). Major trauma is associated with a greater risk of other complications (eg, hypoxic-ischemic encephalopathy and seizures). (See 'Epidemiology' above.)

Risk factors ‒ These include macrosomia (fetal weight greater than 4000 grams), preterm birth, maternal obesity, breech presentation, operative vaginal delivery (ie, the use of forceps or vacuum during delivery) (table 1), small maternal size, and maternal pelvic anomalies. Whether cesarean delivery is a protective factor compared with vaginal delivery is uncertain. (See 'Risk factors' above.)

Site of care – Many neonatal birth injuries can be managed in the well-baby nursery. Neonates with more significant injuries and clinical instability should be monitored in care settings with full cardiopulmonary monitoring and support. (See 'Site of care' above.)

Head injuries These include intracranial hemorrhages (ICH; subdural, subarachnoid, epidural, and intraventricular hemorrhage) and extracranial injuries (subgaleal hemorrhage [SGH], skull fracture, cephalohematoma, and caput succedaneum) (figure 1) (see 'Initial evaluation of head injury' above):

When to suspect ICH ‒ ICH should be suspected in neonates with risk factors (eg, forceps- or vacuum-assisted delivery) who present with vital sign abnormalities, a bulging fontanelle, apnea, respiratory distress, seizures, hypotonia, or decreased consciousness. Diagnosis is made by imaging. Medical management and the decision for neurosurgical intervention are based on the clinical condition of the patient (eg, evidence of increased intracranial pressure) and the nature and size of the injury (algorithm 1). (See 'Intracranial hemorrhage' above.)

Differentiation of extracranial injuries ‒ In neonates without concern for ICH, physical features can usually distinguish the type and extent of extracranial injury (figure 1). Imaging is usually unnecessary except in cases of diagnostic uncertainty or if more significant injury (eg, diffuse scalp edema suggestive of SGH or palpable skull indentation suggestive of fracture) is suspected (algorithm 1).

Early recognition of SGH (image 1) is important to survival, and depressed skull fractures >1 cm warrant evaluation for associated ICH. In contrast to caput succedaneum, cephalohematoma does not extend across suture lines, and both usually resolve spontaneously without intervention. Neonates with cephalohematoma should be assessed for hyperbilirubinemia. (See 'Extracranial injuries' above.)

Limb injury – Limb injuries include fractures (clavicular, humeral, femoral), dislocations, and nerve injury (see 'Injuries to the limbs' above):

When to suspect injury – Significant limb injury should be suspected in neonates with risk factors (eg, breech presentation, shoulder dystocia, macrosomia) who present with abnormal positioning of the extremities and asymmetric or decreased neonatal reflexes or movement of the extremities. Severe injury may present with more rapid onset of symptoms or associated symptoms such as respiratory distress and asymmetric bone contour or crepitation. (See 'Initial evaluation of limb injury' above.)

Evaluation and management – Fractures are diagnosed by obtaining plain radiographs of the affected area; however, ultrasound or MRI may be needed to differentiate between epiphyseal fractures and dislocations. Clavicular fractures are the most commonly reported fracture type and generally do not require intervention; these injuries can usually be managed with observation alone. Dislocations caused by birth trauma are rare and generally warrant orthopedic evaluation. (See 'Fractures' above and 'Dislocations' above.)

Brachial plexus injury with or without phrenic nerve injury (table 2) is one of the most common neurologic birth injuries and can be associated with other limb injuries. This is discussed in detail separately. (See "Neonatal brachial plexus palsy" and "Diaphragmatic paralysis in the newborn".)  

Other injuries – Other injuries resulting from birth trauma include superficial skin bruising, petechiae, subcutaneous fat necrosis (picture 1 and picture 2); nasal septal dislocation; and ocular, intraabdominal, spinal cord, and facial and laryngeal nerve trauma. Although rare, spinal cord and intra-abdominal injuries may result in poor prognosis and require more immediate medical or surgical intervention. The other injuries typically resolve with time but may require intervention if more severe. (See 'Superficial injuries to the skin and soft tissue' above and 'Injuries to the face and neck' above and 'Injuries to the spinal cord' above and 'Injuries to the abdomen' above.)

  1. Gupta R, Cabacungan ET. Neonatal Birth Trauma: Analysis of Yearly Trends, Risk Factors, and Outcomes. J Pediatr 2021; 238:174.
  2. Moczygemba CK, Paramsothy P, Meikle S, et al. Route of delivery and neonatal birth trauma. Am J Obstet Gynecol 2010; 202:361.e1.
  3. Boulet SL, Alexander GR, Salihu HM, Pass M. Macrosomic births in the united states: determinants, outcomes, and proposed grades of risk. Am J Obstet Gynecol 2003; 188:1372.
  4. Nassar AH, Usta IM, Khalil AM, et al. Fetal macrosomia (> or =4500 g): perinatal outcome of 231 cases according to the mode of delivery. J Perinatol 2003; 23:136.
  5. Morris S, Cassidy N, Stephens M, et al. Birth-associated femoral fractures: incidence and outcome. J Pediatr Orthop 2002; 22:27.
  6. Wei C, Stevens J, Harrison S, et al. Fractures in a tertiary Neonatal Intensive Care Unit in Wales. Acta Paediatr 2012; 101:587.
  7. Cedergren MI. Maternal morbid obesity and the risk of adverse pregnancy outcome. Obstet Gynecol 2004; 103:219.
  8. Hughes CA, Harley EH, Milmoe G, et al. Birth trauma in the head and neck. Arch Otolaryngol Head Neck Surg 1999; 125:193.
  9. Rosenberg A. Traumatic birth injury. NeoReviews 2003; 4:270.
  10. Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2022; 150.
  11. Alexander JM, Leveno KJ, Hauth J, et al. Fetal injury associated with cesarean delivery. Obstet Gynecol 2006; 108:885.
  12. Dessole S, Cosmi E, Balata A, et al. Accidental fetal lacerations during cesarean delivery: experience in an Italian level III university hospital. Am J Obstet Gynecol 2004; 191:1673.
  13. Pollina J, Dias MS, Li V, et al. Cranial birth injuries in term newborn infants. Pediatr Neurosurg 2001; 35:113.
  14. Towner D, Castro MA, Eby-Wilkens E, Gilbert WM. Effect of mode of delivery in nulliparous women on neonatal intracranial injury. N Engl J Med 1999; 341:1709.
  15. Demissie K, Rhoads GG, Smulian JC, et al. Operative vaginal delivery and neonatal and infant adverse outcomes: population based retrospective analysis. BMJ 2004; 329:24.
  16. Krishnan V, Jaganathan S, Choudhary AK, et al. Birth-related subdural hemorrhage in asymptomatic neonates: evolution over time and differentiation from traumatic subdural hemorrhage. Pediatr Radiol 2024; 54:1631.
  17. Looney CB, Smith JK, Merck LH, et al. Intracranial hemorrhage in asymptomatic neonates: prevalence on MR images and relationship to obstetric and neonatal risk factors. Radiology 2007; 242:535.
  18. Nikam RM, Kandula VV, Yue X, et al. Birth-related subdural hemorrhage: prevalence and imaging morphology. Pediatr Radiol 2021; 51:939.
  19. Davis DJ. Neonatal subgaleal hemorrhage: diagnosis and management. CMAJ 2001; 164:1452.
  20. Chaturvedi A, Chaturvedi A, Stanescu AL, et al. Mechanical birth-related trauma to the neonate: An imaging perspective. Insights Imaging 2018; 9:103.
  21. Siegel DH, Holland K, Phillips RJ, et al. Erosive pustular dermatosis of the scalp after perinatal scalp injury. Pediatr Dermatol 2006; 23:533.
  22. Anshelevich A, Osterhoudt KC, Introcaso CE, Treat JR. Picture of the month--quiz case. Halo scalp ring. Arch Pediatr Adolesc Med 2010; 164:673.
  23. Rawal S, Modi N, Lacey S, Keane M. Escherichia coli septicaemia arising as a result of an infected caput succedaneum. Eur J Pediatr 2006; 165:66.
  24. Chung HY, Chung JY, Lee DG, et al. Surgical treatment of ossified cephalhematoma. J Craniofac Surg 2004; 15:774.
  25. Wong CH, Foo CL, Seow WT. Calcified cephalohematoma: classification, indications for surgery and techniques. J Craniofac Surg 2006; 17:970.
  26. Chen MH, Yang JC, Huang JS, Chen MH. MRI features of an infected cephalhaematoma in a neonate. J Clin Neurosci 2006; 13:849.
  27. Chan MS, Wong YC, Lau SP, et al. MRI and CT findings of infected cephalhaematoma complicated by skull vault osteomyelitis, transverse venous sinus thrombosis and cerebellar haemorrhage. Pediatr Radiol 2002; 32:376.
  28. Plauché WC. Subgaleal hematoma. A complication of instrumental delivery. JAMA 1980; 244:1597.
  29. Amar AP, Aryan HE, Meltzer HS, Levy ML. Neonatal subgaleal hematoma causing brain compression: report of two cases and review of the literature. Neurosurgery 2003; 52:1470.
  30. Gebremariam A. Subgaleal haemorrhage: risk factors and neurological and developmental outcome in survivors. Ann Trop Paediatr 1999; 19:45.
  31. Kilani RA, Wetmore J. Neonatal subgaleal hematoma: presentation and outcome--radiological findings and factors associated with mortality. Am J Perinatol 2006; 23:41.
  32. Uchil D, Arulkumaran S. Neonatal subgaleal hemorrhage and its relationship to delivery by vacuum extraction. Obstet Gynecol Surv 2003; 58:687.
  33. Dupuis O, Silveira R, Dupont C, et al. Comparison of "instrument-associated" and "spontaneous" obstetric depressed skull fractures in a cohort of 68 neonates. Am J Obstet Gynecol 2005; 192:165.
  34. Agrawal SK, Kumar P, Sundaram V. Congenital depression of the skull in neonate: a case of successful conservative management. J Child Neurol 2010; 25:387.
  35. Arocho-Quinones EV, Lew SM, Foy AB. Vacuum-assisted elevation of pediatric ping-pong skull fractures: a case series and technical note. J Neurosurg Pediatr 2021; 27:325.
  36. Rooks VJ, Eaton JP, Ruess L, et al. Prevalence and evolution of intracranial hemorrhage in asymptomatic term infants. AJNR Am J Neuroradiol 2008; 29:1082.
  37. Högberg U, Andersson J, Squier W, et al. Epidemiology of subdural haemorrhage during infancy: A population-based register study. PLoS One 2018; 13:e0206340.
  38. Whitby EH, Griffiths PD, Rutter S, et al. Frequency and natural history of subdural haemorrhages in babies and relation to obstetric factors. Lancet 2004; 363:846.
  39. Chamnanvanakij S, Rollins N, Perlman JM. Subdural hematoma in term infants. Pediatr Neurol 2002; 26:301.
  40. Huang AH, Robertson RL. Spontaneous superficial parenchymal and leptomeningeal hemorrhage in term neonates. AJNR Am J Neuroradiol 2004; 25:469.
  41. Heyman R, Heckly A, Magagi J, et al. Intracranial epidural hematoma in newborn infants: clinical study of 15 cases. Neurosurgery 2005; 57:924.
  42. Park SH, Hwang SK. Surgical treatment of subacute epidural hematoma caused by a vacuum extraction with skull fracture and cephalohematoma in a neonate. Pediatr Neurosurg 2006; 42:270.
  43. Negishi H, Lee Y, Itoh K, et al. Nonsurgical management of epidural hematoma in neonates. Pediatr Neurol 1989; 5:253.
  44. Hayden CK Jr, Shattuck KE, Richardson CJ, et al. Subependymal germinal matrix hemorrhage in full-term neonates. Pediatrics 1985; 75:714.
  45. Podoshin L, Gertner R, Fradis M, Berger A. Incidence and treatment of deviation of nasal septum in newborns. Ear Nose Throat J 1991; 70:485.
  46. Sooknundun M, Kacker SK, Bhatia R, Deka RC. Nasal septal deviation: effective intervention and long term follow-up. Int J Pediatr Otorhinolaryngol 1986; 12:65.
  47. Holden R, Morsman DG, Davidek GM, et al. External ocular trauma in instrumental and normal deliveries. Br J Obstet Gynaecol 1992; 99:132.
  48. Rehm A, Promod P, Ogilvy-Stuart A. Obstetric neonatal brachial plexus and facial nerve injuries: A 17 years single tertiary maternity hospital experience. Eur J Obstet Gynecol Reprod Biol 2019; 243:57.
  49. Menticoglou SM, Perlman M, Manning FA. High cervical spinal cord injury in neonates delivered with forceps: report of 15 cases. Obstet Gynecol 1995; 86:589.
  50. Kalanjiyam GP, Kanna RM, Rajasekaran S. Pediatric spinal injuries- current concepts. J Clin Orthop Trauma 2023; 38:102122.
  51. Karthikeyan V, Breitbart SC, Malhotra AK, et al. Management of perinatal cervical spine injury using custom-fabricated external orthoses: design considerations, narrative literature review, and experience from the Hospital for Sick Children. Illustrative cases. J Neurosurg Case Lessons 2023; 5.
  52. Uhing MR. Management of birth injuries. Pediatr Clin North Am 2004; 51:1169.
  53. Share JC, Pursley D, Teele RL. Unsuspected hepatic injury in the neonate--diagnosis by ultrasonography. Pediatr Radiol 1990; 20:320.
  54. Oppenheim WL, Davis A, Growdon WA, et al. Clavicle fractures in the newborn. Clin Orthop Relat Res 1990; :176.
  55. Broker FH, Burbach T. Ultrasonic diagnosis of separation of the proximal humeral epiphysis in the newborn. J Bone Joint Surg Am 1990; 72:187.
  56. Paige ML, Port RB. Separation of the distal humeral epiphysis in the neonate. A combined clinical and roentgenographic diagnosis. Am J Dis Child 1985; 139:1203.
  57. Sawant MR, Narayanan S, O'Neill K, Hudson I. Distal humeral epiphysis fracture separation in neonates -- diagnosis using MRI scan. Injury 2002; 33:179.
  58. Jones GP, Seguin J, Shiels WE 2nd. Salter-Harris II fracture of the proximal humerus in a preterm infant. Am J Perinatol 2003; 20:249.
  59. Beall MH, Ross MG. Clavicle fracture in labor: risk factors and associated morbidities. J Perinatol 2001; 21:513.
  60. Hsu TY, Hung FC, Lu YJ, et al. Neonatal clavicular fracture: clinical analysis of incidence, predisposing factors, diagnosis, and outcome. Am J Perinatol 2002; 19:17.
  61. Lam MH, Wong GY, Lao TT. Reappraisal of neonatal clavicular fracture: relationship between infant size and neonatal morbidity. Obstet Gynecol 2002; 100:115.
  62. Assouto C, Bertoncelli CM, Gauci MO, et al. Congenital pseudarthrosis of the clavicle: a systematic review. Int Orthop 2022; 46:2577.
  63. Carvalho M, Barreto MI, Cabral J, et al. Neonatal upper limb fractures - a narrative overview of the literature. BMC Pediatr 2024; 24:59.
  64. Bhat BV, Kumar A, Oumachigui A. Bone injuries during delivery. Indian J Pediatr 1994; 61:401.
  65. Caviglia H, Garrido CP, Palazzi FF, Meana NV. Pediatric fractures of the humerus. Clin Orthop Relat Res 2005; :49.
  66. Nadas S, Gudinchet F, Capasso P, Reinberg O. Predisposing factors in obstetrical fractures. Skeletal Radiol 1993; 22:195.
  67. Thompson KA, Satin AJ, Gherman RB. Spiral fracture of the radius: an unusual case of shoulder dystocia-associated morbidity. Obstet Gynecol 2003; 102:36.
  68. Dunkow P, Willett MJ, Bayam L. Fracture of the humeral diaphysis in the neonate. J Obstet Gynaecol 2005; 25:510.
  69. Anglen JO, Choi L. Treatment options in pediatric femoral shaft fractures. J Orthop Trauma 2005; 19:724.
  70. Schmelzer-Schmied N, Ochs BG, Carstens C. [Shoulder dislocation in the newborn. Report of 12 cases and review of the literature]. Orthopade 2005; 34:454.
  71. Sudesh P, Rangdal S, Bali K, et al. True congenital dislocation of shoulder: A case report and review of the literature. Int J Shoulder Surg 2010; 4:102.
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References