‫بسم هللا الرحمن الرحيم‬

‫‪Birth Injury‬‬
Birth Injury
 Definition: The term birth injury is used
to denote avoidable and unavoidable
mechanical and anoxic trauma incurred by
the infant during labor and delivery.
Birth Injury
Predisposing factors
Maternal factors: Primiparity, small maternal
stature, or maternal pelvic anomalies.
Delivery factors: Prolonged or extremely rapid
labor, or use of midforceps or vacuum extraction.
Fetal factors: Prematurity, fetal macrosomia, or
abnormal presentation (i.e. breech).
Cranial Injuries
Cephalhematoma Caput succedaneum
 Differentiation between Caput Succedaneum and
Cephalhematoma

Cephalhematoma Caput Succedaneum Item

Subperiosteal hematoma Serosanginous infiltration of Composition
(between the bone and its skin and subcutaneous tissue
periosteum) of the scalp
Any bone, usually the Over the presenting site Site
parietal bone
Few hours after birth At birth Onset of appearance
Firm, feeling of depressed Soft, edematous Consistency
fracture on palpation of the
calcified rim
Localized over the bone Diffuse crossing the suture Extent
lines
2 wk-3 months Few days Resolution
Anemia and jaundice if large Ecchymotic skin patches Associated with
Management of anemia and Nothing Management
hyperbilirubinemia
3. Erythema, abrasions, and
ecchymoses of the skin.
4. Subconjunctival hemorrhage and
petechiae of the skin of the head and
neck:

They are common secondary to

increased intrathoracic pressure
during delivery of the chest
 5. Fractures of the skull:

They may occur due to pressure from

forceps or from maternal symphysis
pubis, sacral promontory, or ischial
spines.
Intracranial Hemorrhages (ICH)
Incidence: ICH often involves the ventricles
(intraventricular hemorrhage, IVH). The
incidence of IVH increases with decreasing
birthweight and gestational age: 60-70% of 500-
750 gm infants and 10-20% of 1,000-1,500 gm
infants.
Sites: Bleeding within the skull can occur:
1. Extra cerebrally: Epidural, subdural, or
subarachnoid spaces.
2. Into the parenchyma of the cerebrum or
cerebellum.
3. Into the ventricles from subependymal germinal
matrix.
Etiological factors
1. Trauma: It occurs especially in precipitate
labor, prolonged or difficult labor, breech
delivery, forceps or ventouse delivery, increased
manipulation of the newborn, and when the fetal
head is large in proportion to the size of pelvic
outlet.
2. Hypoxic-ischemic injury to germinal matrix
or its vessels.
3. Congenital vascular anomalies.
4. Primary hemorrhagic disturbance:
Thrombocytopenia, DIC, or hemophilia of the
newborn.
 Clinical manifestations
Onset: Usually within the first 3 days of life and 10-
15% after the 1st wk of life.
1. Signs of blood loss: Pallor, shock, unconjugated
hyperbilirubinemia, and respiratory distress.
2. Manifestations of increased intracranial pressure:
Bulging and tense anterior fontanel and increasing
head circumference, weakness, hypotonia,
seizures, lethargy, irritability, failure to suck well,
high-pitched cry, muscular twitching, and
temperature instability.
3. Manifestations of intracerebral hemorrhage
(if present)
A. Focal neurologic signs: Focal seizures or hemiparesis.
B. Coma.
Diagnosis
1. History.
2. Clinical manifestations.
3. Laboratory data
A. A significant fall in hematocrite without
evidence of hemolysis should suggest either
ICH or subcapsular hemorrhage of the liver.
B. Unconjugated hyperbilirubinemia without
evidence of hemolysis.
C. Thrombocytopenia and prolonged PT and PTT
in DIC.
Diagnosis
4. Cerebral ultrasonography (the method of
choice in diagnosis)
A. Routine: It is done for preterm babies less than
1,500 gm weight or gestational age <30 wk,
within the 1st 7-14 days of life, and again at 36-
40 wk postmenstrual age.
B. Otherwise with clinical manifestations.
5. CT scan or MRI: The stress associated with
transport is a relative contraindication to the
test.
Prognosis
1. Post-hemorrhagic hydrocephalus: Both
communicating (reduced CSF absorption
by arachnoid villi) and obstructive
(reduced CSF outflow through 4th
ventricle).
2. Parenchymal injury: Motor impairments,
educational difficulties, or cerebral palsy.
3. Death: Patients with massive
hemorrhage.
Prevention
1. Judicious management of cephalopelvic
disproportion and operative (forceps or
cesarean section) delivery.
2. Avoid unnecessary manipulations of the
newborns, especially the preterm.
3. Maternal ITP: Antenatal treatment of the
mother by steroids and cesarean section.
Treatment
1. Avoid excessive suctioning and
manipulation.
2. Incubator care: Close observation, O2 for
cyanosis, and good temperature control.
3. Slow administration of fresh whole blood
in cases of anemia or shock.
4. Vitamin K administration.
5. Anticonvulsant drugs for seizures.
6. Management of hyperbilirubinemia.
Treatment
7. Management of DIC.
8. Repeat lumbar punctures for relieving
increased intracranial pressure in case of
post-hemorrhagic hydrocephalus.
9. Neurosurgical consultation. .
Peripheral Nerve Injuries
1. Brachial plexus injury
It occurs when lateral traction is exerted
on the head and neck during delivery of
the shoulders in a vertex presentation, or
when the arms are extended over the
head in a breech presentation.
Peripheral Nerve Injuries
Erb’s paralysis
 Site of injury: C5 and C6 nerves.
 Muscles affected: Deltoid, supraspinatus,
infraspinatus, supinator, brachioradialis, and
biceps muscles. Weakness leads to loss of
the power to abduct the arm from the
shoulder, to rotate the arm externally, and to
supinate the forearm.
 The characteristic position: Adduction and
internal rotation of the arm and pronation of
the forearm.
Erb's Palsy
Motor manifestations
A. Weakness, hypotonia, and hyporeflexia
of the affected muscles.
B. Moro reflex is absent on the affected
side.
C. The hand grasp is preserved (favorable
prognostic sign) unless C7, C8, and T1
nerves are also injured.
D. Diaphragmatic palsy occurs if C4 is also
injured (fluroscopy can detect it).
Motor manifestations
Sensory manifestations: Loss of sensation over
the outer aspect of the arm.
Prognosis: It depends on the nature of injury.
1. Transient: It occurs in cases of edema or
hemorrhage within the nerve sheath.
2. Permanent: It occurs in case of laceration of
nerve fibers.
 Motor manifestations
Treatment
1. Positioning and partial immobilization
90o adduction and external rotation of the arm,
with full supination of the forearm.
2. Physiotherapy: Gentle massage and range
motion exercises are started on the 2nd wk.
3. Surgical (neuroplasty and tendon transfers): It
is indicated if no improvement.
2. Facial nerve palsy
It occurs as a result of pressure on the 7th nerve in
utero, during labor, or from forceps.
It is manifested as LMNL with complete paralysis of
the same side of the face.
The prognosis of the peripheral injury:
Improvement when edema or hemorrhage is
present within the nerve fibers. Neuroplasty is
indicated if the nerve fibers are torn.
Care of the exposed eye is essential (artificial
tears drops).
Facial Nerve Palsy of the Newborn
Injury of the Visceral Organs
1. Liver
The Predisposing factors: Large infant's size,
asphyxia, and hepatomegaly.
Etiology
A. Pressure on the liver during head delivery in
breech presentation.
B. Incorrect cardiac massage.
Pathology: Rupture of the liver with formation of
large subcapsular hematoma.
Injury of the Visceral Organs
Clinical manifestations
A. The infant usually appears normal for the first 1-
3 days.
B. Manifestations of blood loss: Pallor, jaundice,
tachycardia, tachypnea, poor feeding and
lethargy. Shock and death occur if the
hematoma breaks through the capsule into
peritoneal cavity.
C. A mass may be palpable in the right upper
quadrant of abdomen.
Injury of the Visceral Organs
Diagnosis: Clinical manifestations and
ultrasonography.
Treatment
A. Blood transfusion in marked anemia
and/or shock.
B. Exchange transfusion in marked
jaundice.
C. Surgical repair may be required.
Injury of the Visceral Organs
2. Spleen
A. Injury may occur alone or in association
with liver injury.
B. Causes, clinical manifestations, and
treatment are similar to those of liver
injury.
 Injury of the Visceral Organs
3. Adrenal gland
Causes: Usually after breech delivery, trauma,
anoxia, overwhelming infections.
Clinical manifestations
A. Profound shock and cyanosis (acute adrenal
failure).
B. Jaundice and pallor.
C. A mass may be palpable in the flank.
D. Calcified adrenal hematoma may be discovered
accidentally on X-ray.
Diagnosis: Abdominal ultrasonography.
Treatment of acute adrenal failure.
 Injury of Sternocleidomastoid Muscle
(SCM)
Etiology: Bleeding occurs within the muscle
tissue as the result of muscle or fascia disruption
during delivery.
Pathology: Hematoma formation appears few
hours after delivery. Later on, fibrosis leads to
shortening of the muscle and torticollis.
Diagnosis: A palpable mass in SCM muscle.
Treatment: Physiotherapy. Recovery usually
occurs after 3-4 mo.
Fractures
 Any bone may be fractured and any joint may be
dislocated in cases of difficult delivery.
 Fracture clavicle is more frequently occurring
than any other bone as a result of difficult
delivery of shoulders in vertex or breech
presentations.
 The infant doesn’t move the arm with absent
Moro reflex on the same side and crepitus and
bony irregularity may be palpated.
 Immobilization of the limb on the same side is
indicated.
 The prognosis is excellent.
 Perinatal Asphyxia, Hypoxic-Ischemic
Encephalopathy (HIE)
Definitions
 Anoxia: The consequences of a complete lack of
oxygen.
 Hypoxia: An arterial concentration of oxygen is
less than normal.
 Ischemia: Blood flow to cells or organs is
insufficient to maintain their normal function.
 Perinatal asphyxia is an insult to the fetus or
newborn due to lack of oxygen (hypoxia) and/or
lack of perfusion (ischemia) to various organs.
 Hypoxic-ischemic encephalopathy is the
primary cause of permanent damage to CNS cells
which may result in death or which may manifest
later as cerebral palsy or mental retardation.
 Etiology
I. Fetal hypoxia (placental insufficiency) (90% of
causes)
1. Maternal hypoventilation (leading to reduced PaO2
of maternal blood). It may occur during
anesthesia, cyanotic heart disease, or respiratory
failure of the mother.
2. Maternal hypotension: Spinal anesthesia,
compression of vena cava and aorta by gravid
uterus, or dehydration.
3. Uterine causes: Uterine tetany due to excessive
oxytocin dose, leading to reduced placental filling,
or uterine vessel vasoconstriction by cocaine.
4. Umbilical cord: Compression or knotting.
5. Placental: a. Premature separation.
b. Placental insufficiency (toxemia).
 Etiology
II. Neonatal hypoxia (10% of causes).
1. Severe anemia: Hemolysis or hemorrhage.
2. Shock: Adrenal or intracranial hemorrhage,
overwhelming infection, or massive blood loss.
3. CNS depression: Narcosis, injury, or
anomalies.
4. Pulmonary: Respiratory distress syndrome and
others.
5. Congenital cyanotic heart diseases.
Pathology
1. Cortical necrosis or infarcts (focal or
multifocal): Neuronal death resulting in cystic
encephalomalacia (gray mater injury) that
produce focal seizures and hemiplegia. Infarcts
are best visualized with CT scanning or MRI.
2. Periventricular leukomalacia (PVL):
Periventricular white mater injury. Cerebral
edema can be detected by cranial
ultrasonography.
Clinical manifestations of HIE
1. The presence of yellow meconium-
stained amniotic fluid is evidence that fetal
distress has occurred.
2. The neurological manifestations: The
infants are frequently depressed and fail to
breathe spontaneously. Pallor, cyanosis, apnea,
a slow heart rate, seizures, and
unresponsiveness to stimulation are common.
3. The clinical manifestations of other
organs affected by perinatal asphyxia
 Multi-organ Affection due to Asphyxia

Effect System
Myocardial ischemia, poor contractility, tricuspid Cardiovascular
insufficiency, hypotension
Pulmonary hypertension, pulmonary hemorrhage,
respiratory distress syndrome
Acute tubular or cortical necrosis (acute renal failure)
Pulmonary
Adrenal hemorrhage
Perforation, ulceration with hemorrhage, necrosis Renal
Hypoglycemia, hypocalcemia Adrenal
Subcutaneous fat necrosis
Gastrointestinal
Disseminated intravascular coagulopathy
Metabolic
Skin
Hematology
Prevention
Prevention of fetal hypoxia by monitoring the fetal
conditions and maternal O2 supply.
Management
Perinatal management
1. Monitoring of fetal well being during
pregnancy and labor.
2. Resuscitation in the delivery room.

3. Treatment of meconium aspiration.

Postnatal management of asphyxia

I. Investigations
1. EEG: It is indicated to detect seizure foci.
2. Ultrasonic examination: It can be done
early to detect associated hemorrhage and
extent of edema.
3. CT scan:
Early (2-4 days) to detect the extent of edema.
Late (2-4 wk) to detect the extent of
cerebral injury.
Postnatal management of asphyxia
II. Treatment
1. O2 level: Hypoxia should be treated with O2
supply and/or assisted ventilation.
2. Perfusion: Dobutamine (inotropic drug) can
be used to help perfusion.
3. Glucose level: Keep it at 75-100 mg/ dL.
Hypoglycemia may lead to convulsion.
4. Temperature and calcium level should be kept
in a normal range.
Postnatal management of asphyxia

II. Treatment
5. Seizures: They should be controlled by
anticonvulsant drugs as seizures may
lead to energy failure and intracranial
hemorrhage due to increased blood
pressure.
6. Cerebral edema: Avoid fluid overload by
reducing the fluid intake to volume that
equals insensible water loss and urine
output = about 60 mL/ kg/ day.
Postnatal management of asphyxia
II. Treatment
7. Management of the cardiac effects of asphyxia:
Adequate ventilation with correction of
hypoxemia, acidosis, and hypoglycemia.
Volume overload must be avoided. Dopamine
and/or dobutamine are used in case of cardiac
collapse.
8. Management of the renal effects of asphyxia:
Monitoring of urine output, urinalysis, urine
specific gravity, and urine and serum osmolarity
and electrolytes. Measurement of the renal
failure index to help confirm the renal failure.
Dopamine infusion at 1.25-2.5 g per kg per
hour IV may aid renal perfusion.
Postnatal management of asphyxia

II. Treatment
9. Management of the gastrointestinal effects of
asphyxia: We usually do not feed severely
asphyxiated infants for 5-7 days after the insult
or until good bowel sounds are heard and stools
are negative for blood (necrotizing
enterocolitis).
10. Management of the hematological effects of
asphyxia: Management of DIC.
11. Management of the pulmonary effects of
asphyxia: Oxygenation and ventilation
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