Lecture 01 Asphyxia of the newborn.  Birth trauma

 

ASPHYXIA

 

Asphyxia is incapacity of newborn to begin or to support spontaneous respiration after delivery due to breaching of oxygenation during labor and delivery (WHO). According to another definition, asphyxia  - is absense or ineffective respiration of newborn of 1 minute old with Apgar score less than 4.

Asphyxia: means “a stopping of the pulse”, but more useful is a definition of impaired or interrupted gas exchange. These situations can take place:

·        Intrauterine: the gas exchange depends on the function of placenta, and the blood-flow in the umbilical vessels.

·        Postnatal: after delivery the gas exchange takes place in the pulmonary vesicles or alveoli and depends on the function of the heart, lungs and brain.

Causes of Asphyxia.

Fetal hypoxia:

·        Mother: hypoventilation during anesthesia, cyanotic heart disease, respiratory failure or carbon monoxide poisoning.

·        Low maternal blood pressure as a result of the hypotension that may cause compression of the vena cava & aorta by the gravid uterus

·        Premature separation of the placenta; placenta previa

·        Impedance to the circulation of blood through the umbilical cord as a result of compression or knotting of the cord

·        Uterine vessel vasoconstriction by cocaine, smoking

·        Placental insufficiency from numerous causes, including gestosis, eclampcia, toxemia, postmaturity

·        Extremes in maternal age (< 20 years or >35 years)

·        Preterm or postterm gestation.

Intrapartus asphyxia:

·        More frequently inadequate obstetric aid

·        Using forceps, vacuum extraction, cresteller, caesarean section (immediate)

·        Trauma: narrow pelvis, malpresentation

·        Extremely rapid or prolonged labor

·        Multiple gestation

·        Drugs depression of CNS: anesthesia, sedatives & analgesics

·        Meconium-stained amniotic fluid

Postnatal hypoxia:

·        Anemia due to severe hemorrhage or hemolytic disease

·        Shock from adrenal hemorrhage, intraventricular hemorrhage, overwhelming infection, massive blood loss

·        Failure to breathe due to a cerebral defect, narcosis or  injury

·        Failure of oxygenation resulting from of cyanotic congenital heart disease or deficient pulmonary function

Predisposing risk factors for asphyxia are:

·        Multiple gestation;

·        Placental abruption;

·        Placenta previa;

·        Preeclampsia;

·        Meconium-stained amniotic fluid;

·        Fetal bradycardia;

·        Prolonged rupture of fetal membranes;

·        Extremes in maternal age (senior 35 y, junior 20 y);

·        Maternal diabetes;

·        Maternal use of illicit drugs;

 

Apgar Score of the Newborn Apgar score

 

Symptoms

Evaluation

0

1

2

Heart rate (frequency per 1 min.)

Absent

<100 beats/min

>100 beats/min

Respiratory effort

Absent

Weak, irregular

Strong cry

Muscle tone

Hanging down limbs

Slight flexion of limbs

Active movements

Reflex irritability (reaction on nasal catheter, soles’ irritation)

No reaction

Grimace

Cough, sneezing and cry

Skin colour

Generalized paleness or generalized cyanosis

Pink color of body and cyanotic of limbs

Pink color of body and limbs

 

POSTNATAL SYMPTOMS OF ASPHYXIA

MILD ASPHYXIA

The infant who experiences mild asphyxia initially will be depressed. This is followed by a period of hyperalertness, which resolves within 1 or 2 days. 

Clinical symptoms:

·        hyperalertness (jitteriness),

·         increased irritability and tendon reflexes,

·        exaggerated Moro response;

There are no focal signs.

The prognosis is excellent for normal (good) outcome.

 

MODERATE ASPHYXIA

The infant who experiences moderate asphyxia will be very  depressed. This is followed by a prolonged period of hyperalertness and hyperreflexia.   

Clinical symptoms:

·         lethargy, hypotonia

·         suppressed reflexes with or without seizures

·        Generalised seizures often occur 12 to 24 hours after episode of asphyxia, but are controlled easily, resolving in a few days regarding of therapy. 

The prognosis is variable (20-40% with abnormal outcome).

 

SEVERE ASPHYXIA

·        Severe metabolic or mix acidosis pH ≤ 7.00 in arterial blood of umbilical vessels; 

·        Assessment by Apgar is 0-3 during more than 5 minutes;

·        Neurological symptoms such as general hypotonia, lethargy, coma, seizures, brainstem, autonomous dysfunction;

·        Evidence of multiorgan system dysfunction in the immediate neonatal period - damage of vital organs (lungs, heart and others) in fetus or newbon;

·        Severe asphyxia is associated with coma, intractable seizures activity, cerebral oedema, intracranial haemorrhage.

·         The infant often became progressively more depressed over the first 1 to 3 days, as a cerebral oedema develops, and death may occur during this period.

·         Survival is usually associated with poor long-term outcome (100% with abnormal outcome).

Acute complications associated with asphyxia

·        hypoxic-ischemic encephalopathy (HIE)

·        hypotension

·        seizures

·        persistent pulmonary hypertension

·        hypoxic cardiomyopathy

·         necrotizing enterocolitis

·        acute tubular necrosis

·        adrenal hemorrhage and necrosis

·        Hypoglycemia, polycytemia

·        disseminated intravascular coagulation

 

HYPOXIC-ISCHEMIC CEREBRAL INJURY –  HIE

(HYPOXIC-ISCHEMIC ENCEPHALOPATHY)

 

Hypoxic-ischemic encephalopathy s caused by a combination of hypoxemia, ischemia, that results in a decreased supply of oxygen to cerebral tissue. During perinatal asphyxia, birth trauma,  hypercapnia and acidosis may contribute further to the cerebral insult.

Etiology

Most neonatal encephalopathic or seizure disorders, in the absence of major congenital malformations or syndromes, appear to be due to perinatal events. Brain MRI findings in full-term neonates with encephalopathy demonstrate that 80% have acute injuries, <1% have prenatal injuries, and 3% have non–hypoxic-ischemic diagnoses.

Pathophysiology and Pathology

The topography of injury typically correlates with areas of decreased cerebral blood flow. After an episode of hypoxia and ischemia, anaerobic metabolism occurs and generates increased amounts of lactate and inorganic phosphates. Excitatory and toxic amino acids, particularly glutamate, accumulate in the damaged tissue. Increased amounts of intracellular sodium and calcium may result in tissue swelling and cerebral edema. There is also increased production of free radicals and nitric oxide in these tissues. The initial circulatory response of the fetus is increased shunting through the ductus venosus, ductus arteriosus, and foramen ovale, with transient maintenance of perfusion of the brain, heart, and adrenals in preference to the lungs, liver, kidneys, and intestine.

The pathology of hypoxia-ischemia depends on the affected organ and the severity of the injury. Early congestion, fluid leak from increased capillary permeability, and endothelial cell swelling may then lead to signs of coagulation necrosis and cell death. Congestion and petechiae are seen in the pericardium, pleura, thymus, heart, adrenals, and meninges. Prolonged intrauterine hypoxia may result in inadequate perfusion of the periventricular white matter, resulting, in turn, in PVL. Pulmonary arteriole smooth muscle hyperplasia may develop, which predisposes the infant to pulmonary hypertension. If fetal distress produces gasping, the amniotic fluid contents (meconium, squames, lanugo) are aspirated into the trachea or lungs.

Clinical Manifestations

Intrauterine growth restriction with increased vascular resistance may be the 1st indication of fetal hypoxia. During labor, the fetal heart rate slows and beat-to-beat variability declines. Continuous heart rate recording may reveal a variable or late deceleration pattern. Particularly in infants near term, these signs should lead to the administration of high concentrations of oxygen to the mother and consideration of immediate delivery to avoid fetal death and CNS damage.

At delivery, the presence of meconium-stained amniotic fluid is evidence that fetal distress has occurred.

At birth, affected infants may be depressed and may fail to breathe spontaneously. During the ensuing hours, they may remain hypotonic or change from a hypotonic to a hypertonic state, or their tone may appear normal. Pallor, cyanosis, apnea, a slow heart rate, and unresponsiveness to stimulation are also signs of HIE. Cerebral edema may develop during the next 24 hours and result in profound brainstem depression. During this time, seizure activity may occur; it may be severe and refractory to the usual doses of anticonvulsants. Though most often a result of the HIE, seizures in asphyxiated newborns may also be due to hypocalcemia, hypoglycemia, or infection.

HYPOXIC-ISCHEMIC ENCEPHALOPATHY IN TERM INFANTS

modified from Sarnat HB, Sarnat MS

SIGNS

STAGE 1

STAGE 2

STAGE 3

Level of consciousness

Hyperalert

Lethargic

Stuporous, coma

Muscle tone

Normal

Hypotonic

Flaccid

Posture

Normal

Flexion

Decerebrate

Tendon reflexes/clonus

Hyperactive

Hyperactive

Absent

Myoclonus

Present

Present

Absent

Moro reflex

Strong

Weak

Absent

Pupils

Mydriasis

Miosis

Unequal, poor light reflex

Seizures

None

Common

Decerebration

Electroencephalographic findings

Normal

Low voltage changing to seizure activity

Burst suppression to isoelectric

Duration

<24 hr if progresses; otherwise, may remain normal

24 hr-14 days

Days to weeks

Outcome

Good

Variable

Death, severe deficits

 

In addition to CNS dysfunction, heart failure and cardiogenic shock, persistent pulmonary hypertension, respiratory distress syndrome, gastrointestinal perforation, hematuria, and acute tubular necrosis are associated with perinatal asphyxia secondary to inadequate perfusion.

The severity of neonatal encephalopathy depends on the duration and timing of injury. Symptoms develop over a series of days, making it important to perform serial neurologic examinations. During the initial hours after an insult, infants have a depressed level of consciousness. Periodic breathing with apnea or bradycardia is present, but cranial nerve functions are often spared with intact pupillary responses and spontaneous eye movement. Seizures are common with extensive injury. Hypotonia is also common as an early manifestation.

Diagnosis

·        Diffusion-weighted MRI is the preferred imaging modality in neonates with HIE because of its increased sensitivity and specificity early in the process and its ability to outline the topography of the lesion.

·        CT scans are helpful in identifying focal hemorrhagic lesions, diffuse cortical injury, and damage to the basal ganglia; CT has limited ability to identify cortical injury during the 1st few days of life.

·        Ultrasonography has limited utility in evaluation of hypoxic injury in the term infant; it is the preferred modality in evaluation of the preterm infant.

·        Amplitude-integrated electroencephalography (aEEG) may help to determine which infants are at highest risk for long-term brain injury. A single-channel tracing is generated from 2 electrodes placed in the biparietal area. A filter is used to filter and attenuate the signal between 2 Hz and 15 Hz. This technique is simple to perform and correlates with standard EEG. The technique provides information quickly within the window during which intervention is most likely to be useful. Also, aEEG is able to detect seizure activity, which is common in patients with HIE. Continuous aEEG monitoring detects subclinical seizure activity during the subacute phase.

Treatment

Selective cerebral or whole body (systemic) therapeutic hypothermia reduces mortality or major neurodevelopmental impairment in term and near-term infants with HIE. Hypothermia decreases the rate of apoptosis and suppresses production of mediators known to be neurotoxic, including extracellular glutamate, free radicals, nitric oxide, and lactate. The neuroprotective effects are thought to be secondary to downregulation of the secondary mediators of injury resulting from cerebral edema, accumulation of cytokines, and seizures.

Phenobarbital, the drug of choice for seizures, is given with an intravenous loading dose (20 mg/kg); additional doses of 5-10 mg/kg (up to 40-50 mg/kg total) may be needed. Phenytoin (20 mg/kg loading dose) or lorazepam (0.1 mg/kg) may be needed for refractory seizures. Phenobarbital levels should be monitored 24 hours after the loading dose has been given and maintenance therapy (5 mg/kg/24hr) is begun. Therapeutic phenobarbital levels are 20-40 mg/mL. There is some clinical evidence that high-dose prophylactic phenobarbital may decrease neurodevelopmental impairment in infants with HIE.

Additional therapy for infants with HIE includes supportive care directed at management of organ system dysfunction. Hyperthermia has been found to be associated with impaired neurodevelopment, so it is important to prevent hyperthermia before initiation of hypothermia. Careful attention to ventilatory status and adequate oxygenation, blood pressure, hemodynamic status, acid-base balance, and possible infection is important. Secondary hypoxia or hypotension due to complications of HIE must be prevented. Aggressive treatment of seizures is critical and may necessitate continuous EEG monitoring.

 

BIRTH TRAUMA

 

The term “Birth trauma” is used to denote mechanical and anoxic trauma incurred by the infant during labor and delivery. The process of birth is associated with compressions, contractions, and tractions. When fetal size, presentation or neurological immaturity complicate this event, such intrapartum forces may lead to

·        tissue damage,

·        edema,

·        hemorrhage

·        fracture in the neonate.

The risk factor of birth injury

·        Small maternal stature

·        Maternal pelvic anomalies

·        Extremely rapid

·        Prolonged labor

·        Using forceps, vacuum extraction

·        Versions and extraction

·        Deep transverse arrest of descent of presenting part of fetus

·        Oligohydramnions

·        Abnormal presentation (i.e. breech)

·        Very low birth weight infant or extreme premature

·        Postmature infant(> 42 week of gestation)

·        Cesarean section

·        Fetal macrosomia

·        Large fetal head

·        Fetal anomalies

Predisposing factors for brain injury include chronic and acute maternal illness resulting in uteroplacental dysfunction, intrauterine infection, macrosomia/dystocia, malpresentation, prematurity, and intrauterine growth restriction. Acute and often unavoidable emergencies during the delivery process frequently result in mechanical and/or hypoxic-ischemic brain injury.

Classification of birth injuries

I. Soft-tissue injuries

- caput succedaneum

- subcutaneous and retinal hemorrhage, petechia

- ecchymoses and subcutaneous fat necrosis

II. Cranial injuries

- cephalohematoma

- fractures of the skull

III.           Intracranial hemorrhage

-         subdural hemorrhage

-         subarachnoid hemorrhage

-         intra- and periventricular hemorrhage

-         parenchyma hemorrhage

IV. Spine and spinal cord

-         fractures of vertebra

-         Erb-Duchenne paralysis

-         Klumpke paralyses

-         Phrenic nerve paralyses

-          Facial nerves palsy

V.               Peripheral nerve injuries

VI.           Viscera (rupture of liver, spleen and adrenal hemorrhage)

VII.         Fractures of bones.

Caput succedaneum is a diffuse, sometimes ecchymotic, edematous swelling of the soft tissues of the scalp involving the area presenting during vertex delivery. 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 are frequently associated with caput succedaneum and become more evident after the caput has receded; they disappear during the 1st weeks of life. Rarely, a hemorrhagic caput may result in shock and require blood transfusion. Analogous swelling, discoloration, and distortion of the face are seen in face presentations. No specific treatment is needed, but if extensive ecchymoses are present, hyperbilirubinemia may develop.

Petechiae and ecchymosis are common manifestation of birth trauma in the newborn. Petechiae of the skin of the head and neck are common. These lesions resolve spontaneously within 1 week. They are caused by a sudden increase in intrathoracic pressure during labor when the fetus passes through the birth canal. They are temporary and are the result of normal course of delivery. If the etiology is uncertain, studies to rule out coagulation disorders or infections etiology are indicated.

Cephalohematoma is a subperiosteal hemorrhage, hence always limited to the surface of one cranial bone. Cephalohematomas occur in 1-2% of live births. No discoloration of the overlying scalp occurs, and swelling is not usually visible for several hours after birth because subperiosteal bleeding is a slow process. The lesion becomes a firm tense mass with a palpable rim localized over one area of the skull. Most cephalohematomas are resorbed within 2 wk-3 mo, depending on their size. They may begin to calcify by the end of the 2nd week. A few remain for years as bony protuberances and are detectable on radiographs as widening of the diploic space; cystlike defects may persist for months or years. An underlying skull fracture, usually linear and not depressed, may be associated with 10-25% of cases. A sensation of central depression suggesting but not indicative of an underlying fracture or bony defect is usually encountered on palpation of the organized rim of a cephalohematoma. Cephalohematomas require no treatment, although phototherapy may be necessary to treat hyperbilirubinemia. Infection of the hematoma is a very rare complication.

Fractures of the skull may occur as a result of pressure from forceps or from the maternal symphysis pubis, sacral promontory, or ischial spines. Linear fractures, the most common, cause no symptoms and require no treatment. Depressed fractures are usually indentations of the calvaria similar to the dents in a ping-pong ball; they are generally a complication of forceps delivery or fetal compression. Affected infants may be asymptomatic unless they have associated intracranial injury; it is advisable to elevate severe depressions to prevent cortical injury from sustained pressure. Fracture of the occipital bone with separation of the basal and squamous portions almost invariably causes fatal hemorrhage because of disruption of the underlying vascular sinuses. Such fractures may result during breech deliveries from traction on the hyperextended spine of the infant while the head is fixed in the maternal pelvis.

Traumatic epidural, subdural, or subarachnoid hemorrhage is especially likely when the fetal head is large in proportion to the size of the mother's pelvic outlet, with prolonged labor, in breech or precipitous deliveries, or as a result of mechanical assistance with delivery. Massive subdural hemorrhage, often associated with tears in the tentorium cerebelli or, less frequently, in the falx cerebri, is rare but is encountered more often in full-term than in premature infants. Patients with massive hemorrhage caused by tears of the tentorium or falx cerebri rapidly deteriorate and may die soon after birth. The majority of subdural and epidural hemorrhages resolve without intervention; consultation with a neurosurgeon is recommended. The diagnosis of subdural hemorrhage may be delayed until the chronic subdural fluid volume expands and produces megalocephaly, frontal bossing, a bulging fontanel, anemia, and, sometimes, seizures. CT scan and MRI are useful imaging techniques to confirm these diagnoses. Symptomatic subdural hemorrhage in large term infants should be treated by removal of the subdural fluid collection with a needle placed through the lateral margin of the anterior fontanelle. In addition to birth trauma, child abuse must be suspected in all infants with subdural effusion after the immediate neonatal period.

Subarachnoid hemorrhage (SAH) is rare and typically is clinically silent. The anastomoses between the penetrating leptomeningeal arteries or the bridging veins are the most likely source of the bleeding. The majority of affected infants have no clinical symptoms, but the SAH may be detected because of an elevated number of red blood cells in a lumbar puncture sample. Some infants experience benign seizures, which tend to occur on the 2nd day of life. Rarely, an infant has a life-threatening catastrophic hemorrhage and dies. There are usually no neurologic abnormalities during the acute episode or on follow-up. Significant neurologic findings should suggest an arteriovenous malformation; this lesion can easily be detected on CT or MRI; ultrasonography is a less sensitive tool.

 

Intracranial-Intraventricular Hemorrhage and Periventricular Leukomalacia

Etiology

Intracranial hemorrhage usually develops spontaneously; less commonly, it may be due to trauma or asphyxia, and rarely, it occurs from a primary hemorrhagic disturbance or congenital vascular anomaly. Intracranial hemorrhage often involves the ventricles (intraventricular hemorrhage [IVH]) of premature infants delivered spontaneously without apparent trauma. Primary hemorrhagic disturbances and vascular malformations are rare and usually give rise to subarachnoid or intracerebral hemorrhage. In utero hemorrhage associated with maternal idiopathic or, more often, fetal alloimmune thrombocytopenia may occur as severe cerebral hemorrhage or a porencephalic cyst after resolution of a fetal cortical hemorrhage. Intracranial bleeding may be associated with disseminated intravascular coagulopathy, isoimmune thrombocytopenia, and neonatal vitamin K deficiency, especially in infants born to mothers receiving phenobarbital or phenytoin.

Pathogenesis

The major neuropathologic lesions associated with VLBW (VLBW) infants are IVH and periventricular leukomalacia (PVL). IVH in premature infants occurs in the gelatinous subependymal germinal matrix. This periventricular area is the site of origin for embryonal neurons and fetal glial cells, which migrate outwardly to the cortex. Immature blood vessels in this highly vascular region of the developing brain combined with poor tissue vascular support predispose premature infants to hemorrhage. The germinal matrix involutes as the infant approaches full-term gestation and the tissue's vascular integrity improves; therefore IVH is much less common in the term infant. Periventricular hemorrhagic infarction often develops after a grade IVH owing to venous congestion.

Predisposing factors for IVH include prematurity, respiratory distress syndrome, hypoxic-ischemic or hypotensive injury, reperfusion injury of damaged vessels, increased or decreased cerebral blood flow, reduced vascular integrity, increased venous pressure, pneumothorax, thrombocytopenia, hypervolemia, and hypertension.

Understanding of the pathogenesis of PVL is evolving, and it appears to involve both intrauterine and postnatal events. A complex interaction exists between the development of the cerebral vasculature and the regulation of cerebral blood flow (both of which are gestational age dependent), disturbances in the oligodendrocyte precursors required for myelination, and maternal/fetal infection and/or inflammation. Similar factors (hypoxia-ischemia), venous obstruction from an IVH, or undetected fetal stress may result in decreased perfusion to the brain, leading in turn to periventricular hemorrhage and necrosis. PVL is characterized by focal necrotic lesions in the periventricular white matter and/or more diffuse white matter damage. The risk for PVL increases in infants with severe IVH and/or ventriculomegaly. The corticospinal tracts descend through the periventricular white matter, hence the association between cerebral white matter injury/PVL and motor abnormalities, including cerebral palsy.

Clinical Manifestations

The majority of patients with IVH, including some with moderate to severe hemorrhages, have no clinical symptoms. Some premature infants in whom severe IVH develops may have acute deterioration on the 2nd or 3rd day of life. Hypotension, apnea, pallor, or cyanosis; poor suck; abnormal eye signs; a high-pitched, shrill cry; convulsions, or decreased muscle tone; metabolic acidosis; shock; and a decreased hematocrit or failure of the hematocrit to increase after transfusion may be the 1st clinical indications. IVH may rarely manifest at birth; 50% of cases are diagnosed within the 1st day of life, and up to 75% within the 1st 3 days. A small percentage of infants have late hemorrhage, between days 14 and 30. IVH as a primary event is rare after the 1st month of life.

PVL is usually clinically asymptomatic until the neurologic sequelae of white matter damage become apparent in later infancy as spastic motor deficits. PVL may be present at birth but usually occurs later as an early echodense phase (3-10 days of life), followed by the typical echolucent (cystic) phase (14-20 days of life).

The severity of hemorrhage may be defined on CT scans by the location and degree of ventricular dilatation. In a grade I hemorrhage, bleeding is isolated to the subependymal area. In Grade II hemorrhage, there is bleeding within the ventricle but without evidence of ventricular dilatation. Grade III hemorrhage consists of IVH with ventricular dilatation. In Grade IV hemorrhage, there is intraventricular and parenchymal hemorrhage. Another grading system describes 3 levels of increasing severity of IVH detected on ultrasound: In grade I, bleeding is confined to the germinal matrix–subependymal region or to <10% of the ventricle (≈35% of IVH cases); grade II is defined as intraventricular bleeding with 10-50% filling of the ventricle (≈40% of IVH cases) and in grade III, more than 50% of the ventricle is involved, with dilated ventricles (Fig. 93-3). Ventriculomegaly is defined as mild (0.5-1 cm), moderate (1.0-1.5 cm), or severe (>1.5 cm).

Diagnosis

Intracranial hemorrhage is suspected on the basis of the history, clinical manifestations, and knowledge of the birthweight-specific risks for IVH. The associated clinical signs of IVH are typically nonspecific or absent; therefore, it is recommended that premature infants <32 wk of gestation be evaluated with routine real-time cranial ultrasonography through the anterior fontanel to screen for IVH. Infants <1,000 g are at highest risk and should undergo cranial ultrasonography within the 1st 3-7 days of age, when approximately 75% of lesions will be detectable. Ultrasonography is the preferred imaging technique for screening because it is noninvasive, portable, reproducible, and sensitive and specific for detection of IVH.

Ultrasonography also detects the precystic and cystic symmetric lesions of PVL and the asymmetric intraparenchymal echogenic lesions of cortical hemorrhagic infarction. Furthermore, the delayed development of cortical atrophy, porencephaly, and the severity, progression, or regression of posthemorrhagic hydrocephalus can be determined by serial ultrasonographic examinations.

Approximately 3-5% of VLBW infants have posthemorrhagic hydrocephalus and require ventriculoperitoneal shunt insertion; if the initial ultrasonography findings are abnormal, additional interval ultrasonographic studies are indicated to monitor for the development of hydrocephalus.

IVH represents only one facet of brain injury in the term or preterm infant. MRI is a more sensitive tool for evaluation of extensive periventricular injury and may be more predictive of adverse long-term outcome. CT or, more reliably, diffusion-weighted MRI is indicated for term infants in whom brain injury or stroke is suspected, because ultrasonography may not reveal edema or intraparenchymal hemorrhage and infarction.

Prevention

Improved perinatal care is imperative to minimize traumatic brain injury and decrease the risk of preterm delivery. The incidence of traumatic intracranial hemorrhage may be reduced by judicious management of cephalopelvic disproportion and operative (forceps, vacuum) delivery. Fetal or neonatal hemorrhage caused by maternal idiopathic thrombocytopenic purpura or alloimmune thrombocytopenia may be reduced by maternal treatment with steroids, intravenous immunoglobulin, fetal platelet transfusion, or cesarean section. Tenacious care of the LBW infant's respiratory status and fluid and electrolyte management—including avoidance of acidosis, hypocarbia, hypoxia, hypotension, wide fluctuations in neonatal blood pressure or Pco2, and pneumothorax—are important factors that may affect the risk for development of IVH and PVL.

A single course of antenatal corticosteroids is recommended in pregnancies 24-34 wk of gestation that are at risk for preterm delivery. Antenatal steroids decrease the risk of death, grade III and IV IVH, and PVL in the neonate. The prophylactic administration of low-dose indomethacin (0.1 mg/kg/day for 3 days) to VLBW preterm infants reduces the incidence of severe IVH.

Treatment

Although no treatment is available for IVH, it may be associated with other complications that require therapy. Seizures should be treated with anticonvulsant drugs. Anemia and coagulopathy require transfusion with packed red blood cells or fresh frozen plasma. Shock and acidosis are treated with the judicious and slow administration of sodium bicarbonate and fluid resuscitation.

Insertion of a ventriculoperitoneal shunt is the preferred method to treat progressive and symptomatic posthemorrhagic hydrocephalus; some infants require temporary cerebrospinal fluid diversion before a permanent shunt can be safety inserted. Diuretics and acetazolamide are not effective. Serial lumbar punctures, ventricular taps or reservoirs, and externalized ventricular drains are potential temporizing interventions; they have an associated risk of infection and of “puncture porencephaly” owing to injury to the surrounding parenchyma. A ventriculosubgaleal shunt inserted from the ventricle into a surgically created subgaleal pocket provides a closed system for constant ventricular decompression without these additional risk factors. Decompression is regulated by the pressure gradient between the ventricle and the subgaleal pocket.

Brachial Palsy

Brachial plexus injury is a common problem, with an incidence of 0.6-4.6/1,000 live births. Injury to the brachial plexus may cause paralysis of the upper part of the arm with or without paralysis of the forearm or hand or, more commonly, paralysis of the entire arm. These injuries occur in macrosomic infants and when lateral traction is exerted on the head and neck during delivery of the shoulder in a vertex presentation, when the arms are extended over the head in a breech presentation, or when excessive traction is placed on the shoulders. Approximately 45% of brachial plexus injuries are associated with shoulder dystocia.

In Erb-Duchenne paralysis, the injury is limited to the 5th and 6th cervical nerves. The infant loses the power to abduct the arm from the shoulder, rotate the arm externally, and supinate the forearm. The characteristic position consists of adduction and internal rotation of the arm with pronation of the forearm. Power to extend the forearm is retained, but the biceps reflex is absent; the Moro reflex is absent on the affected side. The outer aspect of the arm may have some sensory impairment. Power in the forearm and hand grasps is preserved unless the lower part of the plexus is also injured; the presence of hand grasp is a favorable prognostic sign. When the injury includes the phrenic nerve, alteration in diaphragmatic excursion may be observed with ultrasonography or fluoroscopy.

Klumpke paralysis is a rare form of brachial palsy, in which injury to the 7th and 8th cervical nerves and the 1st thoracic nerve produces a paralyzed hand and ipsilateral ptosis and miosis (Horner syndrome) if the sympathetic fibers of the 1st thoracic root are also injured. Mild cases may not be detected immediately after birth. Differentiation must be made from cerebral injury; from fracture, dislocation, or epiphyseal separation of the humerus; and from fracture of the clavicle. MRI demonstrates nerve root rupture or avulsion.

Full recovery occurs in most patients; prognosis depends on whether the nerve was merely injured or was lacerated. If the paralysis was due to edema and hemorrhage about the nerve fibers, function should return within a few months; if it was due to laceration, permanent damage may result. Involvement of the deltoid is usually the most serious problem and may result in shoulder drop secondary to muscle atrophy. In general, paralysis of the upper part of the arm has a better prognosis than paralysis of the lower part.

Treatment consists of initial conservative management with monthly follow-up and a decision for surgical intervention by three months if function has not improved. Partial immobilization and appropriate positioning are used to prevent the development of contractures. In upper arm paralysis, the arm should be abducted 90 degrees with external rotation at the shoulder, full supination of the forearm, and slight extension at the wrist with the palm turned toward the face. This position may be achieved with a brace or splint during the 1st 1-2 wk. Immobilization should be intermittent throughout the day while the infant is asleep and between feedings. In lower arm or hand paralysis, the wrist should be splinted in a neutral position, and padding placed in the fist. When the entire arm is paralyzed, the same treatment principles should be followed. Gentle massage and range-of-motion exercises may be started by 7-10 days of age. Infants should be closely monitored with active and passive corrective exercises. If the paralysis persists without improvement for 3 months, neuroplasty, neurolysis, end-to-end anastomosis, and nerve grafting offer hope for partial recovery.

Phrenic Nerve Paralysis

Phrenic nerve injury (3rd, 4th, 5th cervical nerves) with diaphragmatic paralysis must be considered when cyanosis and irregular and labored respirations develop. Such injuries, usually unilateral, are associated with ipsilateral upper brachial palsy. Because breathing is thoracic in type, the abdomen does not bulge with inspiration. Breath sounds are diminished on the affected side. The thrust of the diaphragm, which may often be felt just under the costal margin on the normal side, is absent on the affected side. The diagnosis is established by ultrasonographic or fluoroscopic examination, which reveals elevation of the diaphragm on the paralyzed side and seesaw movements of the 2 sides of the diaphragm during respiration.

No specific treatment is available; infants should be placed on the involved side and given oxygen if necessary. Initially, intravenous feedings may be needed; later, progressive gavage or oral feeding may be started, depending on the infant's condition. Pulmonary infections are a serious complication. Recovery usually occurs spontaneously by 1-3 mo; rarely, surgical plication of the diaphragm may be indicated.

Facial Nerve Palsy

Facial palsy is usually a peripheral paralysis that results from pressure over the facial nerve in utero, from efforts during labor, or from forceps use during delivery. Rarely, it may result from nuclear agenesis of the facial nerve. Peripheral paralysis is flaccid and, when complete, involves the entire side of the face, including the forehead. When the infant cries, movement occurs only on the nonparalyzed side of the face, and the mouth is drawn to that side. On the affected side the forehead is smooth, the eye cannot be closed, the nasolabial fold is absent, and the corner of the mouth droops. The forehead wrinkles on the affected side with central paralysis because only the lower  of the face is involved. The infant also usually has other manifestations of intracranial injury, most commonly 6th nerve palsy. The prognosis depends on whether the nerve was injured by pressure or the nerve fibers were torn. Improvement occurs within a few weeks in the former instance. Care of the exposed eye is essential. Neuroplasty may be indicated when the paralysis is persistent. Facial palsy may be confused with absence of the depressor muscles of the mouth, which is a benign problem.

 

REFERENCES

1.    Nelson Textbook of  Pediatrics, 19th Edition. - Expert Consult Premium Edition - Enhanced Online Features and Print / by Robert M. Kliegman, MD, Bonita M.D. Stanton, MD, Joseph St. Geme, Nina Schor, MD, PhD and Richard E. Behrman, MD. - 2011. - 2680 p.

2.    Daniel Bernstein, Steven P. Shelov. Pediatrics for medical students. - USA: Lippinkot Williams & Wilkins. – 2008. - 650 p.

3.    KapitanT.V. Propaedeutics of children’s diseases [Textbook for students of higher medical educations]; Fourth edition, updated &translated in English. – Vinnitsa: The State cartographical Factory, 2012. – 808 p.

4.    Pediatric Skills /Jean W. Solomon, Jane Clifford O`Brien/ . USA: Mosby. -  2011. -  630 p.

5.    Pediatrics / Edited by O.V. Tiazhka, T.V. Pochinok, A.M. Antoshkina/ - Vinnytsa: Nova Knyha Publishers, 2011. - 584 p.

6.    www.bookfinder.com/author/american-academy-of-pediatrics

7.    www.emedicine.medscape.com

8.    http://www.nlm.nih.gov/medlineplus/medlineplus.html

9.    www.tdmu.edu.te.ua