BIRTH INJURIES

DEFINITION:
Injuries to the infant that result from mechanical forces (ie, compression, traction)
during the birth process are categorized as birth trauma. Factors responsible for
mechanical injury may coexist with hypoxic-ischemic insult; one may predispose
the infant to the other.
INCIDENCE:
Significant birth injury accounts for fewer than 2% of neonatal deaths and
stillbirths in the United States; it still occurs occasionally and unavoidably, with an
average of 6-8 injuries per 1000 live births. In general, larger infants are more
susceptible to birth trauma. Higher rates are reported for infants who weigh more
than 4500g.
Most birth traumas are self-limiting and have a favorable outcome. Nearly one half
are potentially avoidable with recognition and anticipation of obstetric risk factors.
Infant outcome is the product of multiple factors. Separating the effects of a
hypoxic-ischemic insult from those of traumatic birth injury is difficult.
Risk factors for birth trauma include the following :

Large-for-date infants, especially infants who weigh more than 4500 g

Instrumental deliveries, especially forceps (midcavity) or vacuum
Vaginal breech delivery
Abnormal or excessive traction during delivery
Occasionally, injury may result from resuscitation. Recognition of trauma
necessitates a careful physical and neurologic evaluation of the infant to establish
whether additional injuries are present. Symmetry of structure and function should
be assessed, the cranial nerves should be examined, and specifics such as
individual joint range of motion and scalp/skull integrity should be evaluated.
ETIOLOGY:
The birth process is a blend of compression, contractions, torques, and traction.
When fetal size, presentation, or neurologic immaturity complicates this event,
such intrapartum forces may lead to tissue damage, edema, hemorrhages, or
fractures in the neonate. The use of obstetric instrumentation may further amplify
the effects of such forces or may induce injury alone. Under certain conditions,
cesarean delivery can be an acceptable alternative but does not guarantee an injuryfree birth. Factors predisposing to injury include the following:

 Prima gravida
Cephalopelvic disproportion, small maternal stature, maternal pelvic
anomalies
Prolonged or rapid labor
Deep, transverse arrest of descent of presenting part of the fetus
Oligohydramnios
Abnormal presentation (breech)
Use of midcavity forceps or vacuum extraction
Versions and extractions
Very low-birth-weight infant or extreme prematurity
Fetal macrosomia
Large fetal head
Fetal anomalies
Injuries with a favorable long-term prognosis
Soft tissue injuries with a favorable long-term prognosis include the following (see
the image below):

Abrasions
Erythema petechia
Ecchymosis
Lacerations

Subcutaneous fat necrosis

Location of injury in
soft tissue planes on the scalp and head.
Skull injuries with a favorable long-term prognosis include the following:

Caput succedaneum
Cephalhematoma
Linear fractures
Facial injuries with a favorable long-term prognosis include the following:

Subconjunctival hemorrhage
Retinal hemorrhage

 Musculoskeletal injuries with a favorable long-term prognosis include

the following:

Clavicular fractures
Fractures of long bones
Sternocleidomastoid injury
Intra-abdominal injuries with a favorable long-term prognosis include
the following:

Liver hematoma
Splenic hematoma
Adrenal hemorrhage
Renal hemorrhage
Peripheral nerve injuries with a favorable long-term prognosis include
the following:

Facial palsy
Unilateral vocal cord paralysis
Radial nerve palsy
Lumbosacral plexus injury

Soft tissue injury is associated with fetal monitoring, particularly with fetal scalp
blood sampling for pH or fetal scalp electrode for fetal heart monitoring, which has
a low incidence of hemorrhage, infection, or abscess at the site of sampling.
Cephalhematoma
Cephalhematoma is a subperiosteal collection of blood secondary to rupture
of blood vessels between the skull and the periosteum; suture lines delineate
its extent. Most commonly parietal, cephalhematoma may occasionally be
observed over the occipital bone.
The extent of hemorrhage may be severe enough to cause anemia and
hypotension, although this is uncommon. The resolving hematoma
predisposes to hyperbilirubinemia. Rarely, cephalhematoma may be a focus
of infection that leads to meningitis or osteomyelitis. Linear skull fractures
may underlie a cephalhematoma (5-20% of cephalhematomas). Resolution
occurs over weeks, occasionally with residual calcification.

 No laboratory studies are usually necessary. Skull radiography or computed

tomography (CT) scanning is performed if neurologic symptoms are present.
Usually, management solely consists of observation. Transfusion for anemia,
hypovolemia, or both is necessary if blood accumulation is significant.
Aspiration is not required for resolution and is likely to increase the risk of
infection.
Hyperbilirubinemia occurs following the breakdown of the red blood cells
(RBCs) within the hematoma. This type of hyperbilirubinemia occurs later
than classic physiologic hyperbilirubinemia. The presence of a bleeding
disorder should be considered. Skull radiography or CT scanning is also
performed if a concomitant depressed skull fracture is a possibility.
Subgaleal hematoma
Subgaleal hematoma is bleeding in the potential space between the skull
periosteum and the scalp galea aponeurosis. Ninety percent of cases result
from a vacuum applied to the head at delivery. Subgaleal hematoma has a
high frequency of occurrence of associated head trauma (40%), such as
intracranial hemorrhage or skull fracture.[4] The occurrence of these features
does not significantly correlate with the severity of subgaleal hemorrhage.[5]
The diagnosis is generally a clinical one, with a fluctuant, boggy mass
developing over the scalp (especially over the occiput). The swelling
develops gradually 12-72 hours after delivery, although it may be noted
immediately after delivery in severe cases. The hematoma spreads across the
whole calvaria; its growth is insidious, and subgaleal hematoma may not be
recognized for hours.
Patients with subgaleal hematoma may present with hemorrhagic shock. The
swelling may obscure the fontanelle and cross suture lines (distinguishing it
from cephalhematoma). Watch for significant hyperbilirubinemia. In the
absence of shock or intracranial injury, the long-term prognosis is generally
good.
Laboratory studies consist of a hematocrit evaluation. Management consists
of vigilant observation over days to detect progression and provide therapy
for such problems as shock and anemia. Transfusion and phototherapy may
be necessary. Investigation for coagulopathy may be indicated.

Caput succedaneum
Caput succedaneum is a serosanguineous, subcutaneous, extraperiosteal
fluid collection with poorly defined margins; it is caused by the pressure of
the presenting part against the dilating cervix. Caput succedaneum extends
across the midline and over suture lines and is associated with head molding.
Caput succedaneum does not usually cause complications and usually
resolves over the first few days. Management consists of observation only.

Abrasions and lacerations

Abrasions and lacerations sometimes may occur as scalpel cuts during
cesarean delivery or during instrumental delivery (ie, vacuum, forceps).
Infection remains a risk, but most of these lesions uneventfully heal.
Management consists of careful cleaning, application of antibiotic ointment,
and observation. Bring edges together using Steri-Strips. Lacerations
occasionally require suturing.
Subcutaneous fat necrosis
Subcutaneous fat necrosis is not usually detected at birth. Irregular, hard,
nonpitting, subcutaneous plaques with overlying dusky, red-purple
discoloration on the extremities, face, trunk, or buttocks may be caused by
pressure during delivery. No treatment is necessary. Subcutaneous fat
necrosis sometimes calcifies.
Peripheral nerve damage in the form of brachial plexus injury occurs most
commonly in large babies, frequently with shoulder dystocia or breech delivery.
Incidence for brachial plexus injury is 0.5-2 per 1000 live births. Most cases are
Erb palsy; entire brachial plexus involvement occurs in 10% of cases.
Traumatic lesions associated with brachial plexus injury include the following:
Fractured clavicle (10%)

 Fractured humerus (10%)

Cervical cord injury (5-10%)
Facial palsy (10-20%)
Medical and nursing management
Management consists of prevention of contractures. Immobilize the limb gently
across the abdomen for the first week and then start passive range-of-motion
exercises at all joints of the limb. Use supportive wrist splints.
The best results from surgical repair appear to be obtained in the first year of
life. Several investigators have recommended surgical exploration and grafting if
no function is present in the upper roots at age 3 months, although the
recommendation for early explorations is far from universal.
Complications of brachial plexus exploration include infection, poor outcome, and
burns from the operating microscope. Patients with root avulsion do not do well.
Palliative procedures involving tendon transfers have been of some use. Results
from a study by Ruchelsman et al of 21 children who suffered brachial plexus birth
injury indicated that patients who have no active wrist extension following the
trauma can be successfully treated with a tendon transfer but that surgical
outcomes tend to be worse in patients with global palsy.
Latissimus dorsi and teres major transfers to the rotator cuff have been advocated
for improved shoulder function in Erb palsy. One permanent and 3 transitory
axillary nerve palsies have been reported from the procedure
Cranial nerve and spinal cord injuries result from hyperextension, traction, and
overstretching with simultaneous rotation; they may range from localized
neurapraxia to complete nerve or cord transection.
Unilateral branches of the facial nerve and vagus nerve, in the form of recurrent
laryngeal nerve, are most commonly involved in cranial nerve injuries and result in
temporary or permanent paralysis.
Compression by the forceps blade has been implicated in some facial nerve injury,
but most facial nerve palsy is unrelated to trauma from obstetric instrumentation
(eg, forceps). The compression appears to occur as the head passes by the sacrum.
Physical findings for central nerve injuries are asymmetrical facies with crying.
The mouth is drawn towards the normal side, wrinkles are deeper on the normal
side, and movement of the forehead and eyelid is unaffected. The paralyzed side is

smooth with a swollen appearance, the nasolabial fold is absent, and the corner of
the mouth droops. No evidence of trauma is present on the face.

NEONATAL SEIZRES:
The most prominent feature of neurologic dysfunction in the neonatal period is the
occurrence of seizures. Determining the underlying etiology for neonatal seizures
is critical
The neonatal period is limited to the first 28 days of life in a term infant. For
premature infants, this term usually is applied until gestational age 44 weeks; ie,
the age of the infant from conception to 44 weeks (ie, 4 wk after term).
Seizure characteristics
Most neonatal seizures occur over only a few days, and fewer than half of affected
infants develop seizures later in life. Such neonatal seizures can be considered
acute reactive (acute symptomatic), and therefore the term neonatal epilepsy is not
used to describe neonatal seizures.
Seizures in neonates are relatively common, with variable clinical manifestations.
Their presence is often the first sign of neurologic dysfunction, and they are
powerful predictors of long-term cognitive and developmental impairment.
Most seizures in the neonate are focal, although generalized seizures have been
described in rare instances.
Subtle seizures are more common in full-term than in premature infants. Video
electroencephalogram (EEG) studies have demonstrated that most subtle seizures
are not associated with electrographic seizures. Examples of subtle seizures include
chewing, pedaling, or ocular movements.
Neonatal seizure classification
Clonic seizures

These movements most commonly are associated with electrographic seizures.

They often involve 1 extremity or 1 side of the body. The rhythm of the clonic
movements is usually slow, at 1-3 movements per second.
Tonic seizures
These may involve 1 extremity or the whole body. Focal tonic seizures involving 1
extremity often are associated with electrographic seizures.
Generalized tonic seizures often manifest with tonic extension of the upper and
lower limbs and also may involve the axial musculature in an opisthotonic fashion.
Generalized tonic seizures mimic decorticate posturing; the majority are not
associated with electrographic seizures.
Myoclonic seizures
These may occur focally in 1 extremity or in several body parts (in which case they
are described as multifocal myoclonic seizures).
Focal and multifocal myoclonic seizures typically are not associated with
electrographic correlates. Generalized myoclonic jerks are possibly the clinical
equivalent of infantile spasms.

DIAGNOSTIC FINDINGS:
Cranial ultrasonography
Cranial ultrasonography is performed readily at the bedside; it is a valuable tool for
quickly ascertaining whether intracranial hemorrhage, particularly intraventricular
hemorrhage, has occurred. A limitation of this study is the poor detection rate of
cortical lesions or subarachnoid blood.
Cranial CT scanning
Cranial computed tomography (CT) scanning is a much more sensitive tool than
ultrasonography in detecting parenchymal abnormalities. The disadvantage is that
the sick neonate must be transported to the imaging site.

A distinct advantage is that with modern CT scan techniques, a study can be

obtained in approximately 10 minutes.
Cranial CT scan can delineate congenital malformations. Subtle malformations
may be missed on CT scan, requiring a magnetic resonance imaging (MRI) study.
MRI
Cranial MRI is the most sensitive imaging study for determining the etiology of
neonatal seizures, particularly when electrolyte imbalance has been excluded as the
seizures cause.[16] A major disadvantage is that MRI cannot be performed quickly
and, in an unstable infant, it is best deferred until the acute clinical situation
resolves.
Echocardiography
This study can rule out cardiac hypomotility as a result of more diffuse hypoxia.
Tests to ascertain the cause of neonatal seizures include the following:
Serum glucose and electrolytes - Transient neonatal hypocalcemia is a cause
of neonatal seizures during the first 3 weeks of life; hypocalcemia associated
with chromosome 22q11 deletion syndrome may also be a consideration
TORCH (toxoplasmosis, rubella, CMV, herpes) infection studies
Urine organic acids
Serum amino acid assay
Renal function tests - These tests rule out posthypnotic renal dysfunction;
hypoxic damage to multiple organ systems may also be suggested by
elevated liver Trans amylase levels.
Cerebrospinal fluid analysis
This should include tests checking for the following:
Pleocytosis
Xanthochromia - Suggestive of blood breakdown products, particularly if
jaundice is not present
Lactic acid and pyruvate - For evidence of mitochondrial cytopathies
Herpes virus - Using a polymerase chain reaction (PCR) assay
Glucose concentration - Low glucose concentration is suggestive of bacterial
meningitis

In the absence of bacterial meningitis, persistently low CSF glucose concentrations

may suggest a glucose transporter defect.
Electroencephalography
Electroencephalography plays a vital role in properly identifying and
differentiating neonatal seizures from nonepileptic events.[10, 11] Video EEG
monitoring may be helpful when infrequent neonatal seizures persist
MEDICAL AND NURSING MANAGEMENT
Acute neonatal seizures should be treated aggressively, although controversy exists
as to the optimal treatment for them.
When clinical seizures are present, a rigorous workup to determine an underlying
etiologic cause should be initiated quickly. Electrolyte imbalances should be
corrected through a central venous site. Hypocalcemia should be treated cautiously
with calcium, since leakage of calcium into subcutaneous tissue can cause scarring.
When an inborn error of metabolism is suspected, discontinue feeding, since
feeding may exacerbate the seizures and encephalopathy. Institute intravenous
solutions.
Once these issues have been addressed, antiepileptic drug (AED) therapy should be
considered. Phenobarbital is the initial drug of choice. If seizures persist, the use of
phenytoin should be considered.

COLLEGE OF NURSING
Madras medical college, Chennai-03

seminar

Programme

Msc (N) II year

Subject

Obstetrics and gynaecological nursing

Topic

Neonatal Jaundice,scizure,Birth
injuries

Submitted to

Mrs.V.Jayanthi,Msc(N),lecturer
College of nursing,
Madras medical,
Chennai-03.

Submitted by

P.Mary Agila

Date

27.09.14