BIRTH INJURIES

Aruna. A P I Year MSc Nursing

DEFINITION
An impairment of the infants body function or structure due to adverse influences that occur at birth (National vital statistics report)

RISK FACTORS
Primiparity Small maternal stature Maternal pelvic anomalies Prolonged or unusually rapid labor Oligohydramnios Malpresentation of the fetus

 Use of mid forceps or vaccum extraction Versions and extractions Very low birth weight or extreme prematurity Fetal macrosomia or large fetal head Fetal anomalies

TYPES
Head and neck injuries Nerve injury Facial injuries Fractures
Intra-abdominal injury

Soft tissue injuries

HEAD AND NECK INJURIES

EXTRACRANIAL INJURIES
CAPUT SUCCEDANEUM CEPHALHEMATOMA SUBGALEAL HEMORRHAGE

CAPUT SUCCEDANEUM
A caput succedaneum is a serosanguinous fluid collection above the periosteum. It presents as a soft tissue swelling with purpura and ecchymosis over the presenting portion of the scalp. It may extend across the midline and across suture lines.

 The edema disappears within the 1st few days of life. Molding of the head and overriding of the parietal bones disappear during the 1st weeks of life. Rarely, a hemorrhagic caput may result in shock and require blood transfusion.

MANAGEMENT
No specific treatment is needed But if extensive ecchymoses are present, hyperbilirubinemia may develop Shock Blood transfusion

CEPHALHEMATOMA
A cephalhematoma is a subperiosteal blood collection caused by rupture of vessels beneath the periosteum.

Clinical features
Swelling, usually over a parietal or occipital bone Swelling does not cross a suture line and is often not associated with discoloration of the overlying scalp. Limited to the surface of one cranial bone.

Diagnosis
Physical examination Skull radiograph cranial computed tomography

 If infection is suspected, aspiration of the mass If sepsis, antibiotics hyperbilirubinemia photo therapy

SUBGALEAL HEMORRHAGE
A subgaleal hemorrhage is bleeding between the galea aponeurosis of the scalp and the periosteum.

FEATURES
A subgaleal hemorrhage presents as a firm-to-fluctuant mass that crosses suture lines. The mass is typically noted within 4 hours of birth.

LABORATORY FINDINGS
serial hemoglobin and hematocrit monitoring, coagulation profile to investigate for the presence of a coagulopathy. Bilirubin levels also need to be monitored

TREATMENT
Supportive Transfusions may be required if blood loss is significant. In severe cases, surgery may be required to cauterize the bleeding vessels. These lesions typically resolve over a 23 week period

CRANIAL INJURIES
LINEAR SKULL FRACTURES DEPRESSED SKULL FRACTURES

LINEAR SKULL FRACTURES

Usually affect the parietal bones. The pathogenesis is related to compression from the application of forceps, or from the skull pushing against the maternal symphysis or ischeal spines. Rarely, a linear fracture may be associated with a dural tear, with subsequent development of a leptomeningeal cyst.

DEPRESSED SKULL FRACTURES

Indications for surgery include radiographic evidence of bone fragments in the cerebrum presence of neurologic deficits signs of increased intracranial pressure signs of cerebrospinal fluid beneath the galea failure to respond to closed manipulation.

 Indications for nonsurgical management include Depressions less than 2 cm in width and depressions over a major venous sinus Without neurologic symptoms

INTRACRANIAL INJURY
Intracranial haemorrhage Epidural hemorrhage Subdural hemorrhage Subarachnoid hemorrhage Intraparenchymal haemorrhage Germinal matrix hemorrhage / intraventricular haemorrhage

INTRACRANIAL HAEMORRHAGE
Bleeding can occur
External to the brain into the epidural, subdural or subarachnoid space In to the parenchyma of the cerebrum or cerebellum Into the ventricles from the subependymal germinal matrix or choroid plexus

RISK FACTORS
forceps delivery vacuum extraction precipitous deliver prolonged second stage of labor macrosomia

SYMPTOMS
apnea seizures

EPIDURAL HEMORRHAGE
Epidural hemorrhage primarily arises from injury to the middle meningeal artery, and is frequently associated with a cephalhematoma or skull fracture.

CLINICAL MANIFESTATIONS
Diffuse neurologic symptoms Increased intracranial pressure Bulging fontanels Localized symptoms, Lateralizing seizures Eye deviation.

DIAGNOSIS
cranial computed tomography showing a high-density lentiform lesion in the temporoparietal region Skull radiographs

MANAGEMENT
Surgical management

Aspiration of blood from the accompanying cephalhaematoma

SUBDURAL HEMORRHAGE
most frequent intracranial hemorrhage related to birth trauma

 Laceration of the tentorium, with rupture of the straight sinus, vein of Galen transverse sinus, or infratentorial veins causing a posterior fossa clot and brainstem compression Laceration of the falx, with rupture of the inferior sagittal sinus resulting in a clot in the longitudinal cerebral fissure

 Laceration of the superficial cerebral vein, causing bleeding over the cerebral convexity Occipital osteodiastasis, with rupture of the occipital sinus, resulting in a posterior fossa clot

CLINICAL FEATURES
Respiratory symptoms such as apnea Seizures Focal neurologic deficits Lethargy Hypotonia Other neurologic symptoms

DIAGNOSIS
Cranial computed tomography Cranial ultrasonography MRI. Coagulation profile

SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage is caused by rupture of the bridging veins of the subarachnoid space or small leptomeningeal vessels

MANIFESTATIONS
Seizures, often occurring on the second day of life Irritability Depressed level of consciousness Focal neurologic signs.

DIAGNOSIS
Cranial computed tomography. Cranial ultrasonography Lumbar puncture shows an increased number of red blood cells

MANAGEMENT
Resolves without intervention Monitoring head growth

INTRAPARENCHYMAL HAEMORRHAGE
TYPES Intra cerebral
Causes:

rupture of an av malformation or aneurysm coagulation disturbances extracorporeal membrane oxygenation therapy secondary to a large ICH in any other compartment

 Intracerebellar : more common in preterm than the term babies. May be a primary haemorrhage or may result from venous hemorrhagic infarction or from extension of GMH/ IVH

CLINICAL FEATURES
In the preterm infant
IPH is often clinically silent in either intracranial fossa , unless the hemorrhage is quite large

In the term infant, manifestations are

Seizures Hemiparesis Gaze preference Irritability Depressed level of consciousness

DIAGNOSIS
CT Scans MRI Cranial ultrasonography

MANAGEMENT
Symptomatic treatment and support Neurosurgical intervention

GERMINAL MATRIX HEMORRHAGE

(INTRAVENTRICULAR HAEMORRHAGE)

Causes:
Trauma, Perinatal asphyxia Secondary to venous hemorrhagic infarction in the thalamus

FACTORS IN THE PATHOGENESIS

Intra vascular factors
Ischemia / reperfusion Fluctuating cerebral blood flow Increase in CBF Increase in cerebral venous pressure Platelet dysfunction Coagulation disturbances

 Vascular factors
Tenuous involuting capillaries with large diameter lumen

Extra vascular factors

Deficient vascular support Excessive fibrinolytic activity

CLINICAL FEATURES
In the preterm newborn Usually clinically silent Decreased levels of consciousness and spontaneous movement Hypotonia Abnormal eye movement Skew deviation

In term newborns Seizures Irritability Apnea Lethargy Vomiting with dehydration Full fontanels

DIAGNOSIS
Cranial ultra sonography CT or MRI

MANAGEMENT
Prevention Supportive care Careful monitoring Surgical intervention

NERVE INJURY

BRACHIAL PLEXUS INJURY

Erbs palsy Klumpkespalsy Injury to the upper plexus, Erb-Duchenne paralysis

BRACHIAL PLEXUS INJURY Risk factors

Macrosomia shoulder dystocia instrumented deliveries malpresentation

ERB-DUCHENNE PARALYSIS
5th and 6th cervical nerves injury The infant loses the power to abduct the arm from the shoulder, rotate the arm externally, and supinate the forearm Erbs palsy may also be associated with injury to the phrenic nerve, which is innervated with fibers from C3C5

 Adduction and internal rotation of the arm with pronation of the forearm. Biceps reflex is absent Moro reflex is absent on the affected side. The involved arm is held in the waiters tip position, with adduction and internal rotation of the shoulder, extension of the elbow, pronation of the forearm, and flexion of the wrist and fingers.

KLUMPKESPALSY
Involves the C8 and T1 nerves, resulting in weakness of the intrinsic hand muscles and long flexors of the wrist and fingers

 The grasp reflex is absent but the biceps reflex is present. Flaccid extremity with absent reflexes.

ASSOCIATED LESIONS
Hematomas of the sternocleidomastoid muscle, and fractures of the clavicle and humerus. Ipsilateral Horners syndrome (ptosis, miosis, and anhydrosis) when there is accompanying injury to the sympathetic fibers of T1.

TYPES
Neuropraxia with temporary conduction block Axonotmesis with a severed axon, but with intact surrounding neuronal elements Neurotmesis with complete postganglionic disruption of the nerve Avulsion with preganglionic disconnection from the spinal cord

DIAGNOSIS
Physical examination. Radiographs of the shoulder and upper arm

MANAGEMENT
Initial treatment is conservative. The arm is immobilized across the upper abdomen during the first week Physical therapy with passive range-ofmotion exercises at the shoulder, elbow and wrist should begin after the first week. Infants without recovery by 3 to 6 months of age may be considered for surgical exploration

FACIAL NERVE PALSY (BELLS PALSY)

Risk factors
forceps delivery prolonged second stage of labor

Clinical manifestations
weakness of both upper and lower facial muscles. At rest, the nasolabial fold is flattened and the eye remains persistently open on the affected side. During crying, there is inability to wrinkle the forehead or close the eye on the ipsilateral side, and the mouth is drawn awayfrom the affected side.

 lacerations and bruising neurologic findings

TREATMENT
protection of the involved eye by application of artificial tears and taping to prevent corneal injury. neurosurgical repair of the nerve should be considered only after lack of resolution during 1 year of observation

PHRENIC NERVE INJURY

The phrenic nerve arises from the third through fifth cervical nerve roots. Injury to the phrenic nerve leads to paralysis of the ipsilateral diaphragm.

CLINICAL MANIFESTATIONS
respiratory distress, with diminished breath sounds on the affected side. Chest radiographs show elevation of the affected diaphragm, with mediastinal shift to the contralateral side. Ultrasonography or fluoroscopy can confirm the diagnosis by showing paradoxical diaphragmatic movement during inspiration

TREATMENT
Initial treatment is supportive Oxygen Respiratory failure may be treated with continuous positive airway pressure or mechanical ventilation. Gavage feedings. Plication of the diaphragm

LARYNGEAL NERVE INJURY

Symptoms
Stridor respiratory distress hoarse cry dysphagia, Aspiration

 Diagnosis is made by direct laryngoscopy

Treatment
Small frequent feedings may be required to decrease the risk of aspiration. Intubation Tracheostomy Bilateral paralysis tends to produce more severe distress, and therefore requires intubation and tracheostomy placement more frequently

SPINAL CORD INJURY

Clinical findings decreased or absent spontaneous movement absent deep tendon reflexes absent or periodic breathing lack of response to painful stimuli below the level of the lesion.

 Lesions above C4 are almost always associated with apnea Lesions between C4 and T4 may have respiratory distress secondary to varying degrees of involvement of the phrenic nerve and innervation to the intercostal muscles

MANAGEMENT
If cord injury is suspected in the delivery room, the head, neck, and spine should be immobilized. Therapy is supportive.

FACIAL INJURIES

NASAL SEPTAL DISLOCATION

Nasal septal dislocation involves dislocation of the triangular cartilaginous portion of the septum from the vomerine groove

CLINICAL FEATURES
airway obstruction. deviation of the nose to one side The nares are asymmetric, with flattening of the side of the dislocation (Metzenbaum sign). Application of pressure on the tip of the nose (Jeppesen and Windfeld test) causes collapse of the nostrils, and the deviated septum becomes more apparent.

MANAGEMENT
Definitive diagnosis can be made by rhinoscopy manual reduction performed by an otolaryngologist using a nasal elevator. Reduction should be performed by 3 days of age

OCULAR INJURIES
Rupture of Descemets membrane of the cornea lid lacerations hyphema (blood in anterior chamber) vitreous hemorrhage Purtschers retinopathy corneal edema, corneal abrasion

CONGENITAL MUSCULAR TORTICOLLIS

atrophic muscle fibers surrounded by collagen and fibroblasts. tearing of the muscle fibers or fascial sheath with hematoma formation and subsequent fibrosis.

CLINICAL FEATURES
The head is tilted toward the side of the lesion and rotated to the contralateral side, chin is slightly elevated. If a mass is present, it is firm, spindleshaped, immobile, and located in the midportion of the sternocleidomastoid muscle, without accompanying discoloration or inflammation.

DIAGNOSIS
physical examination Radiographs should be obtained to rule out abnormalities of the cervical spine. Ultrasonography may be useful both diagnostically and prognostically.

TREATMENT
active and passive stretching surgery

FRACTURES

CLAVICULAR FRACTURE
clavicle is the most frequently fractured bone during birth

Risk factors
higher birth weight prolonged second stage of labor shoulder dystocia instrumented deliveries

MANAGEMENT
Asymptomatic incomplete fractures require no treatment. Complete fractures are treated with immobilization of the arm for 7 to 10 days

LONG BONE FRACTURES

Risk factors
breech presentation cesarean delivery low birthweight

CLINICAL FEATURES
decreased movement of the affected extremity, swelling, pain with passive movement, and crepitus

DIAGNOSIS
Diagnosis is made radiographically Ultrasonography

TREATMENT
immobilization and splinting Closed reduction and casting are required only when the bones are displaced. Proximal femoral fractures may require a spica cast or use of a Pavlik harness

INTRA-ABDOMINAL INJURY
Liver injury is the most common Three potential mechanisms lead to intraabdominal injury: (1) direct trauma, (2) compression of the chest against the surface of the spleen or liver (3) chest compression leading to tearing of the ligamentaous insertions of the liver or spleen

CLINICAL MANIFESTATIONS
With hepatic or splenic rupture, patients develop sudden pallor, hemorrhagic shock, abdominal distention, and abdominal discoloration. Presentation of a liver rupture with scrotal swelling and discoloration has been described.

 Subcapsular hematomas may present more insidiously, with anemia, poor feeding, tachypnea, and tachycardia. Adrenal hemorrhage may present as a flank mass

DIAGNOSIS
abdominal ultrasound Computed tomography Abdominal radiographs may show nonspecific intraperitoneal fluid or hepatomegaly. Abdominal paracentesis is diagnostic if a hemoperitoneum is present

TREATMENT
volume replacement and correction of any coagulopathy. If the infant is hemodynamically stable, conservative management is indicated. With rupture or hemodynamic instability, a laparotomy is required to control the bleeding. Patients with adrenal hemorrhage may require hormone replacement therapy.

SOFT TISSUE INJURIES

Petechiae and ecchymoses Lacerations and abrasions Subcutaneous fat necrosis

NURSES ROLE

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