Neonatology

Neonatology

إعداد:د.علي عبد الرزاق

Neonatal period: starts from birth till 28 days of life. Full term newborn: a baby born after 37 weeks of gestation. Preterm(premature) baby: a live born infant before 37 weeks of gestation. Postmature baby: a baby born after 42 weeks of gestation. Low birth weight infant(LBW): infant having birth weight less than 2500g. Very low birth weight infant(VLBW): infant having less than 1500g at birth.

Perinatal mortality rate: The perinatal mortality rate is the number of deaths of fetuses weighing at least 500 g (or after 22 completed weeks of gestation), plus the number of early neonatal deaths, per 1000 total births. Neonatal mortality rate: it includes all infants dying during the period from birth to the first 28 days of life, expressed as the number of deaths per 1000 live births. Infant mortality rate: it includes deaths of infants in the neonatal and post neonatal period, expressed as number of deaths per 1000 live births. Stillborn baby: a baby born without heart beat, apneic, limp, pale and cyanotic. (intrauterine death)

Assessment of newborn baby History taking: antenatal( primary health care visit, medical illness, infection, drug exposure, radiation) and natal history( gestational age, onset of respiration, birth weight), also maternal history of still birth, recurrent abortion. Physical examination: to look for various manifestations of neonatal disease, and to look for any congenital malformations. Appearance: Look for cyanosis, nasal flaring, grunting and intercostal retraction suggest pulmonary disease. Meconium stained umbilical cord, nails and skin, may suggest meconium aspiration.


Vital signs and growth measures: HR: normal 120-160 beats/min RR: normal 30-60 cycles/min Temp. :per rectum or axillary route. Length: normal 50cm Weight: normal 3-3.5 (4.5) kg Head circumference: normal 35cm

Skin examination: Look for pallor, plethora, jaundice, cyanosis, petechiae, congenital nevi and rash. Acrocyanosis (of the feet and hands) which is normal in full term and premature infants in the first day after delivery. Vernix caseosa, a soft white cream layer covering the skin of term infants (not present in preterm). Mongolian blue spots are transient, dark blue pigmented macules over the lower back and buttocks, usually disappear by one year of age. Erythema toxicum: is an erythematous papular- vesicular rash are common in the neonate during the first week of life, it contains eosinophil inside, disappear spontaneously.

Acrocyanosis

Erythema toxicum
Mongolian blue spot
Vernix caseosa



Milia, is a yellow-white epidermal cysts of the pilosebacious follicles that are noted on the nose. Capillary and cavernous hemangiomas may be seen and usually resolves 1-4 years of age. Portwine stain that is seen on the face should consider Sturge Weber syndrome: convulsions, mental sub-normality, and ipsilateral intracranial calcification. Mild edema may be present in premature infants but may suggest hydrops fetalis, hypoalbuminemia, or Turner syndrome. Sclerema: it is a form of hardening of the skin and subcutaneous tissues, it is a sign of septicemia. Hair tufts over the lumbosacral spines suggest spinal cord defects.

Milia

Capillary hemangioma
Portwine stain


Skull: Look for premature fusion of the cranial sutures ( craniostenosis). Size of the fontanels: posterior is small less than 1 cm, anterior is diamond shape measures 1.5x2 cm Causes of large(wide) fontanels: achondroplasia, congenital hypothyroidism, congenital infection, hydrocephaly, osteogenesis imperfecta. Also look for encephalocele, cephalhematoma, caput succedaneum.

Face, eyes and mouth: Look for dysmorphic feature: Epicanthic folds (Down syndrome), low set ears, cleft lip and palate, microphthalmia, cataract (congenital infections or chromosomal disorders) White pupillary reflex may indicates cataract, ocular tumors, severe chorioretinitis, and retinopathy of prematurity. Neck and chest: Periodic breathing is a normal pattern of breathing in newborn, characterized by periods of rapid breathing followed by pause of less than 10 seconds then he resume breathing again. Look for cystic hygroma or sternomastoid tumor in the neck.

Epicanthic fold

Cystic hygroma


Breast abscess or engorgement. Webbing of the neck, widely spaced nipples in Turner syndrome.

Cardiovascular examination: Listen for murmurs(congenital heart disease) or patent ductus arteriosus. Examination of peripheral pulses and look for femoral-radial delay(coarctation of aorta)
Webbing of neck



Abdomen: Liver is usually palpable 1cm below costal margin. Feel for any abdominal mass( hydronephrosis, neuroblastoma). Abdominal distension may suggest meconium ileus, ileal atresia, imperforate anus. Meconium stool should pass within the first 48 hr of birth. Urine should normally pass within the first 24 hr of birth. Umbilical stump should contain 2 arteries and one vein. Look for umbilical hernia, omphalocele( herniation of abdominal content through the umbilical cord)

2 arteries and one vein

Umbilical hernia
omphalocele


Genitalia: Look for patency of anus. The testes should be descendent in a full term infant. Look for hernia, hydrocele, hypospadias. Female genitalia: look for ambiguous genitalia, in which there is hypertrophy of clitoris and labial fusion, which suggest congenital adrenal hyperplasia. Extremities: Look for polydactly( extra finger or digit), syndactly(fusion of the fingers), simian crease( single in Down syndrome) and club feet. Spines: Look for myelomeningocele, hair tuft. Hip joints: examine both hip joints for congenital dysplasia by Barlow's and Ortolani tests.

Ambiguous genitalia

hydrocele
hypospadias
myelomeningocele

Primitive neonatal reflexes: Moro reflex: elicited by sudden, slight dropping of the supported head from a slightly raised supine position, there will be opening of the hands with extension and abduction followed by adduction and flexion. The reflex present at birth and disappear by 3-6 mo of life, its presence beyond 6 mo suggest cerebral palsy. Absent moro reflex: in intracranial birth injury, cerebral depression by narcotics, or anesthesia given to the mother just before delivery. Asymmetric response(unilateral moro reflex) may be seen in brachial plexuses injury or fracture clavicle. Palmer grasp reflex: It present by 28 weeks of gestation and gone by 4 mo of age when voluntary palmer grasp begins.

Rooting reflex: Is the turning of the head toward tactile stimulus of the perioral area. Stepping reflex: When a newborn sole of the foot touches the edge of the table, he will make a step. It disappear by 4 mo of age Tonic neck reflex: Placing the newborn in a supine position, by lateral rotation of the head to one side, there will be ipsilateral extension of the arm and leg with flexion of limbs on the opposite side ( fencing posture). The age of the response is 1-6mo of age. Absent reflex indicates a spinal cord disease.


Routine delivery room care: Newborn should be placed head downward immediately after delivery to clear the mouth, nose and pharynx from fluids, mucus, meconium or blood by gentle suction. Then by gentle tactile stimulation to enhance respiration. Maintenance of body heat: Relative to body weight, the surface area of newborn is three times that of the adult, so the heat loss of newborn is approximately 4 times that of adult. The heat loss occur by: Convection of the heat energy to the cooler surrounding air. Conduction of the heat to the colder materials on which the newborn resting. Radiation of the heat from the infant to other nearby cooler solid objects. Evaporation from moist skin and from lungs.


After birth, the newborn infant begins life covered by amniotic fluid and situated in a cold environment( 20-25 ˚C).An infant skin temperature may fall 0.3 ˚C/min, and the core temperature may decline 0.1 ˚C/min in the delivery room.In the absence of an external heat source, the infant must increase metabolism substantially to maintain body temperature.Hypothermia may lead to metabolic acidosis, hypoxemia, hypoglycemia and increased renal excretion of water and solutes which occur in term infants to compensate for heat loss. Therefore it is important to dry the newborn infant from secretions and fluids immediately after delivery and to put them under radiant heater during resuscitation, while normal term infants should be dried and wrapped in blanket.

Antiseptic skin and umbilical cord care: Careful removal of blood from the skin of newborn may reduce risk of blood born infection. The entire skin and umbilical cord should be cleansed with warm water or mild soap solution and then rinsed with water. Then the newborn is dried and should be wrapped in sterile blanket. Umbilical cord may be treated with bactericidal or antimicrobial agents. Chlorhexidine washing of the skin should be avoided because it may induce neurotoxicity. Rigidly enforcing hand to elbow washing of the nursery personnel with iodophor containing antiseptic soap or chlorhexidine before caring each newborn.

Other measures: Vitamin k should be given as a prophylaxis to all newborn 1mg (IM) for full term and 0.5mg for preterm, to prevent hemorrhagic disease of newborn Then if the newborn in a satisfactory condition, is given to his mother for immediate bonding and feeding.

Small for date infant( intrauterine growth retardation): It describes a newborn who is smaller than the usual number of weeks of gestation, his birth weight at 10th centile for babies of same gestational age. IUGR occurs when the fetus does not receive the necessary nutrients and oxygen needed for proper growth and development of organs and tissues. Clinical features: The weight is most affected while the head circumference is the least. The skin is thick, pale and crackled. If meconium present, the skin, umbilical cord and nails are greenish. There is little subcutaneous fat, decreased muscle mass.

IUGR

larger heads for the size of the body (CNS sparing), widened anterior fontanels. Physical examination should detail the presence of dysmorphic features might suggest underlying congenital malformations, chromosomal defects, or exposure to teratogens.. Hepatosplenomegaly, jaundice, and skin rashes in addition to ocular disorders, such as chorioretinitis, cataracts, glaucoma, and cloudy cornea, suggest the presence of a congenital infection or inborn error of metabolism. Mortality rates of infants severely affected are 5 to 20 times the mortality rates of infants who are appropriate for gestational age.

Post mature( peeling skin, dry) long nails

Causes of LBW or small for date:
C. Placental causes
B. Fetal causes
Maternal factors
Placental tumors. Chronic abruptio placentae. Twin-to-twin transfusion syndrome. Placental insufficiency
Congenital infections( rubella) Chromosomal abnormalities. Congenital malformations. Multiple gestations.
Previous LBW baby Low socioeconomic state Low level of maternal education No antenatal care Maternal age<16yr or>35yr Short interval between pregnancies. Cigarette smoking Physical & psychological Stresses. Low pre pregnancy weight Hypertension, DM, PET.



Problems(complications) of small for date newborn: Temperature instability, mostly hypothermia, due to loss of subcutaneous fat, hypoxia and hypoglycemia. Hypoglycemia, due to decreased glycogen stores, decrease gluconeogenesis, and hypothermia. Polycythemia-hyperviscosity from fetal hypoxia with increased erythropoietin production. Dysmorphology due to syndrome anomalies or chromosomal genetic disorders. Pulmonary hemorrhage due to hypothermia, polycythemia and hypoxia. Meconium aspiration. Perinatal asphyxia due to decreased uteroplacental perfusion during labor or from meconium aspiration.


Preterm infant: A newborn baby who is delivered before 37 weeks of gestation. Characteristic features of prematurity: Thin transparent skin with pitting edema over the dorsum of hands and feet. Small baby but plump. Hypotonic Decrease firmness of ear lobe, decrease size of breast tissues, and few or absent creases over the sole of foot. Underdeveloped genitalia, in male, testes may not be descendent, and wide separation of labia majora not covering the minora in female. Excess lanugo hair over the back, trunk and shoulders. Posture: the more the premature the baby is, the more he is flaccid and the flexion posture not assumed (frog posture).

Preterm babies Extended frog like posture

Lanugo hair

Causes of preterm birth:

Others
Maternal
Uterine
Placental
Fetal
Premature rupture of membrane Polyhydraminios Iatrogenic (CS) 4. trauma
PET DM Hypertension Infection with group B strep. Herpes simplex Syphilis Chorioaminionitis Drug use
Bicornuate uterus Incompetent cervix
Placenta previa. Abruptio placentae.
Fetal distress. Multiple gestations Erythrobl-astosis Congenital anomalies



Problems( complications) of preterm infant: Respiratory distress syndrome and apneic attacks. Metabolic: hypoglycemia, hypocalcaemia and jaundice of prematurity. Hypothermia due to immature thermoregulatory centre, and little subcutaneous fat. Infection and septicemia, due to underdeveloped immune system and excessive instrumentation. Gastrointestinal problems: Poor sucking and swallowing and immature bowel function, and necrotizing enterocolitis.


Neurologic: intraventricular hemorrhage, hypotonia. Retinal problems: retinopathy of prematurity secondary to hyper oxygenation. Cardiovascular problems: bradycardia with apnea, patent ductus arteriosus. Blood problems: exaggeration of physiological anemia, hemorrhage.

Management of premature baby: Thermal control: to keep the infant core temperature 36.5-37C, humidity 40%, inside an incubator care. Oxygen: humidified oxygen in 2-3L/min. 3. Fluid requirement: in the first day of life starts with 70ml/kg, then add 10-20ml/kg daily until it reaches 150ml/kg at fifth day of life. Type of fluid 10% glucose water in the first 2 days of life, then changed to 1/5th glucose saline. Avoid giving excessive fluid because of risk of patent ductus arteriosus.

Feeding: do not give feeding until there is, a good bowel function i.e. passage of meconium, active bowel sounds, no abdominal distension, normal respiration and no apneic attacks and after the baby is clinically stable and can tolerate oral feeding. Bottle feeding is easier than breast feeding for 34 wk old neonate. Nasogastric tube feeding is appropriate for 32wk premature. Prevention of infection: Minimum handling of premature. Avoid excessive instrumentations. Appropriate hand to elbow washing before nursing a preterm baby. Early recognition and treatment of infection.

Immaturity of drug metabolism: Renal excretion is slower than that of older children, so the drug interval should be at least 12 hourly. Prevention of premature birth( also prevention of RDS) By treating the underlying medical conditions and eliminate risk factors that induce preterm labor. Bed rest to the mother, treatment of infections. Pregnant mother is given dexamethasone injection at least 48 hr before premature delivery to lessen the complications

Respiratory distress syndrome( Hyaline membrane disease) RDS: Pathophysiology: The normal mature lung during fetal life secrets a substance from type2 cells called surfactant, which is a phospholipids containing lecithin, it is essential for the stability of the lung, it prevent atelactasis by reducing surface tension in the alveoli at end expiration. In preterm baby this surfactant is deficient, so the surface tension forces of the alveoli are not reduced, therefore atelactasis develops during end expiration as the alveolus collapses leading to decrease functional residual capacity, so hypoxemia, pulmonary artery vasoconstriction and respiratory distress will develop. Factors that further reduce surfactant synthesis include, hypovolemia, acidosis and hypoxemia.


The pathology of (RDS). Infants may recover completely or develop chronic lung damage, resulting in bronchopulmonary dysplasia (BPD). FiO2 = fraction of inspired oxygen; HMD = hyaline membrane disease; V/Q = ventilation perfusion.

Infants at a greater risk for RDS : Prematurity Delivery of previous preterm baby with RDS. Maternal DM. Hypothermia Fetal distress, asphyxia. Male sex, white race. Being a second born of twin.

Clinical manifestations: Tachypnea, cyanosis, nasal flaring, intercostals and subcostal retractions, grunting( caused by closure of the glottis during expiration to maintain adequate gas exchange during exhalation). During next 72 hr baby either show signs of improvement or he may deteriorate into severe respiratory distress, apneic attacks and respiratory failure. Auscultation of the chest show diminished air entry bilaterally. CXR: show atelactasis seen as a ground glass haze in the lung surrounding air-filled bronchi( air bronchogram= aerated bronchioles superimposed on a background of collapsed alveoli) Blood gas analysis show decreased Po2, increase Co2 and low PH.



Chest radiographs in a premature infant with respiratory distress syndrome before and after surfactant treatment. Left: Initial radiograph shows poor lung expansion, air bronchogram, and reticular granular appearance. Right: Repeat chest radiograph obtained when the neonate is aged 3 hours and after surfactant therapy demonstrates marked improvement.


After birth, RDS may be prevented or its severity reduced by early intratracheal administration of surfactant. Differential diagnosis: Early onset sepsis, pneumonia, congenital diaphragmatic hernia, pneumothorax, cyanotic congenital heart disease and lobar emphysema. Treatment of RDS: Adequate humidified oxygen to keep O2 saturation 90%. O2 can be administered by nasal cannula or oxygen hood. The goal of therapy for patients with respiratory distress syndrome is to maintain a pH of 7.25-7.4, a partial pressure of oxygen (PaO2) of 50-70mm Hg, and a carbon dioxide pressure (PCO2) of 40-65 mm Hg.

If hypoxemia( PaO2<50mmHg) present then nasal continuous positive airway pressure should be added. If respiratory failure ensures(Pco2>60mmHg, PH<7.2, PaO2 <50mmHg) with 100% oxygen then assisted ventilation using a respirator is indicated. 10% glucose water is given in the first 2 days then changed to 1/5th glucose saline. Because it is difficult to distinguish between sepsis and pneumonia from RDS, broad spectrum antibiotics using ampicillin and gentamicin is added. Surfactant administration through endotracheal tube will improve alveolar oxygen, increase pulmonary compliance and improve CXR findings. Repeated doses is given every 6-12hr.

Complications of RDS: Pulmonary air leaks: pneumothorax, subcutaneous emphysema and pneumomediastinum. Patent ductus arteriosus(PDA): in term infants the ductus closes within 24-48 hr of birth, while in preterm infant specially with RDS may remain patent. blood will be shunted from left to right direction, causing heart failure, pulmonary edema and machinery murmur ( systolic and diastolic). it can be prevented by initial fluid restriction and diuretic use, if not closed, so give indomethacin IV injection and finally if not closed surgical correction needed later on.


Bronchopulmonary dysplasia: it is a form of chronic lung disease in which there is oxygen dependency. it is caused by oxygen mediated lung damage, manifested by hypercapnea, hypertension, poor growth and right sided HF. Retinopathy of prematurity( Retrolental fibroplasia): it is caused by acute and chronic effects of oxygen toxicity on the developing blood vessels of premature infants retina. it is the leading cause of blindness in very LBW infants. the excessive arterial oxygen tension will cause vasoconstriction of retinal vasculature, this will lead to vaso-obliteration and fibro vascular proliferation with retinal detachment.


Perinatal asphyxia( Hypoxic Ischemic Encephalopathy): It is the state of reduced gaseous exchange through the placenta or through the lungs, leading to lack of oxygen and perfusion to various organs. Pathophysiology: It is a process of hypoxia, hypercapnea, poor cardiac output and metabolic acidosis. Asphyxia associated with severe bradycardia or cardiac insufficiency will lead to ischemia. Fetal and neonatal circulatory system responds to hypoxia by shunting blood preferentially to the brain, heart, adrenals and away from the intestine, kidney, lungs and skin.

The metabolic acidosis during asphyxia is caused by: Poor cardiac output secondary to hypoxic depression of myocardial function. Systemic hypoxia. Tissue anaerobic metabolism. With severe and prolonged asphyxia, multiple vital organs are affected.

Causes of birth asphyxia:

Postpartum
Intrapartum
Intrauterine
CNS may be affected by maternal medications, trauma Congenital neuromuscular disease like cong. Myasthenia gravis, myopathy, myotonic dystrophy. Infection: pneumonia, shock. Airway disorder: choanal atresia, laryngeal webs. Pulmonary disorder: severe immaturity, pneumothorax, pleural effusion, diaphragmatic hernia.
Birth trauma: cephalopelvic disproportion, shoulder dystocia, breech presentation Hypoxia-ischemia: umbilical cord compression, tetanic contraction of uterus.
Hypoxia-ischemia: uteroplacental insufficiency, abruptio placentae, prolapsed cord, maternal hypotension anemia-shock: placenta previa, fetomaternal hemorrhage, erythroblastosis.



Effects(complications) of birth asphyxia: CNS: hypoxic-ischemic encephalopathy(H.I.E), intraventricular hemorrhage, cerebral edema, seizures, hypotonia, hypertonia, later on infant may have delayed development, cerebral palsy and mental retardation. CVS: myocardial ischemia, poor contractility, hypotension. Pulmonary: persistent pulmonary hypertension, RDS. Renal: acute tubular or cortical necrosis. Adrenal: adrenal hemorrhage. GIT: perforation, ulceration, and necrosis. Metabolic: inappropriate ADH secretion, hyponatremia, hypoglycemia, hypocalcaemia. Hematology: DIC.


Apgar score examination: It is a rapid scoring system based on physiological responses to the birth process and it is used to assess the need to resuscitate a newborn. This scoring system is based on 5 physiological criteria, which should be observed by qualified examiner at interval of 1 and 5 min after birth. Full term infant with normal cardiopulmonary adaptation should score 8 to 9 at 1 and 5 min. Apgar score of 4 to 7 warrant close attention Apgar score of 0 to 3 represents either cardiopulmonary arrest, hypoventilation, severe bradycardia or CNS depression.

Apgar scoring parameters:

2
1
0
signs
>100/min
<100/min
0
Heart rate
Vigorous cry
Weak cry
None
Respiration
Arms, legs well flexed
Some extremity flexion
None
Muscle tone
Cry, withdrawal
Some motion
None
Reflex irritability
Pink all over
Pink body, blue extremities
Blue
Body color

APGAR Scoring

Clinically:Early signs of fetal distress, fetal heart rate show deceleration pattern, scalp PH<7.20 and meconium stained liquor.After birth the newborn fail to breath spontaneously and may remain hypotonic, pale, cyanosed, apneic, and unresponsive to stimulation.Other presentations may occur like RDS, HF, pulmonary hypertension, hematuria, convulsion……

Prognosis: Mortality rate 10-20-% Those who recover usually had mild presentations, while those with moderate and severe presentations many of them will have neurological sequel like cerebral palsy, MR, epilepsy, hearing defect, and microcephaly. Investigations: Blood gas analysis, PH. Brain and abdominal ultrasound. CT scan of the brain, to look for infarction, bleeding or intraventricular hemorrhage. EEG later on.

APGAR

7 - 10 Normal Infant Suction oropharnyx Keep warm

APGAR

4 - 6 Moderate asphyxia Suction oropharnyx Keep warm Oxygenate If 5 minute score < 7, repeat every 5 minutes for 20 minutes

APGAR

0 - 3 Asphyxia neonatorum Resuscitate aggressively


Treatment( resuscitation): Systemic or selective cerebral hypothermia for acute management of hypoxic ischemic encephalopathy is promising. The resuscitation usually follows A,B,C,D. A: secure patent airway by gentle oropharyngeal suction of amniotic fluid, meconium or blood. B: maintain breathing through gentle tactile stimulation, oxygen by face mask or ambu bag with positive pressure ventilation. If still there is no spontaneous respiration, HR <100/min, then ventilation is done through endotracheal intubation, with external cardiac massage over the lower third of the sternum at rate of 120/min.


Anticonvulsants is given when indicated, phenobarbitone given IV as 20mg/kg loading dose followed by 5mg/kg maintenance dose, or phenytoin as alternative. Lorazepam 0.1mg/kg/ day may be needed in refractory cases. Good response is determined by Adequate chest rise Symmetric breath sounds Improved pink color HR>100/min and Spontaneous respiration.

Neonatal birth injury Caput succedaneum: It is a diffuse edematous swelling of the soft tissues of the scalp that extends across the suture lines. It may be seen after prolonged labor. It usually resolves spontaneously within few days and need no treatment. Cephalhematoma: It is a subperiosteal hemorrhage that does not cross the suture lines surrounding the respective bone. A linear fracture may be seen underlying a cephalhematoma It may be unilateral or bilateral. With time, cephalhematoma may organize, calcify and form a central depression. Usually it resolves spontaneously without treatment but it may exacerbate neonatal jaundice.

Caput succedaneum

cephalhematoma


Strenomastoid tumor: It is a form of birth injury results from difficult vaginal delivery Excessive traction over the neck of newborn baby may cause injury of the sternomasoid muscle with bleeding and then fibrosis forming a lump inside the muscle. It should be differentiated from cystic hygroma Treatment by simple massage over the affected muscle with physiotherapy. Rare cases may result in torticolis.

Sternomastoid tumor

Intracranial hemorrhage: May result from mechanical trauma due to cephalopelvic disproportion, breech or forceps delivery or may result from anoxia. It is more common in preterm baby than full term. Clinically symptoms appear after few hours, or delayed 1-2 days. The baby is lethargic with poor sucking, or had irritability, high pitched cry, vomiting, weak or absent primitive reflexes, pallor and convulsion. The anterior fontanel may be tens and bulging.

Lumbar puncture show bloody CSF Brain ultrasound or CT scan to localize the site of hemorrhage. Prognosis: death may occur due to respiratory failure, survivors may have neurological sequel like cerebral palsy or hydrocephaly. Treatment is supportive with minimal handling, incubator care, control convulsion and blood transfusion to correct anemia.

Erbs palsy

Klumpkes paralysis: Caused by injury to C7th, C8th and first thoracic nerves, resulting in paralyzed hand, if the sympathetic nerves injured also, ipsilateral horner syndrome occur( ptosis, miosis) Recovery occurs within few weeks or may take several months. Phrenic nerve injury: Injury to C3,C4,C5 nerves will lead to diaphragmatic paralysis and respiratory distress. It may be associated with Erbs palsy. Diagnosis by CXR under fluoroscopy to see the movement of diaphragm.


Facial nerve injury: Most commonly result from compression of facial nerve between the facial bones and the mother pelvic bones or by physicians forceps. There will be asymmetric cry, mouth deviated toward the normal side, eye on the affected side cant be closed and absent nasolabial fold. To differentiate it from central injury (upper motor neuron lesion),in lower motor neuron lesion the lower two third of face and the forehead are affected, while in UMN lesion Only the lower part of the face is affected.

Fracture: Of the clavicle is common, usually unilateral and occur in macrosomic newborn after shoulder dystocia, there will be limitation of movement on the affected side with unilateral moro reflex. Of the skull is rare either linear fracture require no treatment, or depressed, which may need surgical decompression. Extremity fracture is less common and it involves the humerus more than the femur.

Neonatal infections Infections are frequent and important cause of morbidity and mortality in neonate. Risk Factors: Prematurity and low birth weight Maternal GBS Prolonged rupture of membranes(more than 18 hours) Maternal chorioamnionitis Sibling with sepsis Meconium at delivery Need for resuscitation Male child Multiple gestation

Modes of transmission: Intrauterine(transplacental): here the infection transmitted from mother to the fetus through the placenta( congenital infection). Examples: cytomegalovirus( CMV), rubella, toxoplasmosis, syphilis, varicella virus, mycobacterium TB and listeria monocytogens. First trimester infection will lead to congenital malformations e.g. rubella. 3rd trimester infection, often results in active infection at the time of delivery e.g. toxoplasmosis, syphilis. Infection may result in abortion, IUGR, or congenital malformations.


Natal infection( ascending infection): Here the organisms transmitted to the fetus through ascending infection from pathogens in the maternal genital tract after prolonged rupture of membrane>18 hours, or as the newborn pass through birth canal. E.g. group B streptococcus, gonococci, chlamydia, E.coli, HIV, CMV.

postnatal: Here the infection may be transmitted by direct contact with hospital personnel, the mother or family members, from breast milk( like HIV, CMV) .or from contaminated equipment. The most common source of infection in hospitalized newborn is hand contamination of health care personnel. E.g. coagulase negative staphylococcus, E.coli, Klebsiella, salmonella, enterobacter, staph.aureus, Candida.

Congenital infections Congenital toxoplasmosis: It is transferred by vertical transmission through the placenta to the fetus, after acute maternal infection. The risk of infection increases to 90% near term. The severity of fetal disease varies inversely with gestational age at which maternal infection occurs. The newborn may have subclinical infection at birth, or show classic finding, like chorioretinitis, hydrocephaly, small for gestational age, jaundice with hepatosplenomegaly, seizures and maculopapular rash.

X-ray of skull show diffuse cortical calcifications in contrast to CMV infection which causes periventricular calcifications. Diagnosis by serological tests including immunoflourescent antibody test, IgG and IgM specific antibodies that achieve peak concentration 1-2 mo after infection and remain positive indefinitely. Also MRI, CT scan of brain and eye examination. Treatment: pyrimethamin ( with folic acid) and sulphadiazine for up to one year.



Congenital rubella infection: If the infection acquired during the first 4 weeks of gestation. Congenital defects approaches 85% and close to 40% abort spontaneously or stillborn. Infection occurs after 4th mo of gestation doesn't seem to cause disease. Clinical features include: Cataract, retinopathy and glaucoma. Heart: patent ductus arteriosus, peripheral pulmonary artery stenosis. Auditory: sensorineural hearing loss. Neurologic: meningoencephalitis, mental retardation, and behavioral changes. Hematologic: anemia, thrombocytopenia. Growth retardation, hepatosplenomegaly, jaundice, purpuric skin rash and radiolucent bone disease.

Congenital rubella syndrome

Diagnosis: by detection of rubella specific IgM antibodies, usually indicates recent infection. IgG antibodies recovered after several months is confirmatory. Isolation of rubella virus from blood, urine, csf, and throat swab. Infants with congenital infection shed the virus in the stool, urine, and respiratory secretions for up to one year. There is no effective antiviral medications for congenital rubella.


Congenital cytomegalovirus infection( CMV): May be transmitted transplacental or during birth process. It is the most common congenital infection and the leading cause of sensorineural hearing loss, MR, and cerebral palsy. The most common source of maternal infection during pregnancy is via sexual contacts and contact with young infected children. More than 90% of congenital infection is asymptomatic at birth.

10% of infected infants have symptoms like small for gestational age, microcephaly, thrombocytopenia, hepatosplenomegaly, hepatitis, intracranial calcifications( periventricular), chorioretinitis and hearing abnormalities. other infants show the disease later in infancy when they found to have sensorineural hearing loss and developmental delay. CMV infection that is acquired during birth or from mothers milk is not associated with neonatal illness or CNS disease. CMV is relatively sensitive to acyclovir, ganciclovir, they will reduce virus shedding.


Herpes simplex infection: HSV2 account for 90% of primary genital herpes. 70-85% of neonatal herpes simplex infection is caused by HSV2 Infection is acquired from the mother shortly before or during delivery( ascending). Most infants are normal at birth and symptoms develop 5-10 days of life. Disseminated disease involving multiple organs( liver, lung), localized infection to CNS, skin, eyes and mouth. The infection is usually severe and delay in treatment can result in morbidity and mortality. Diagnosis by viral culture from skin vesicles, nasopharynx, eyes, urine, blood, csf, stool and rectum. Treatment: parenteral acyclovir 20mg/kg/dose Q8 hrs 14 days.

Herpes simplex infection

Natal infections It refers to infection that occurs intrapartum( during delivery). Risk factors for natal infection includes: 1- Prolonged rupture of membrane>18 hours, 2- Instrumentations, and 3- Maternal infections (pyrexia). Local infections: Ophthalmia neonatorum: Mainly caused by Chlamydia trachomatis and gonococcus. It is transmitted to the newborn by contact with vaginal secretions during birth.

Gonococcal ophthalmia: Infection is usually present less than 7 days of birth, characterized by clear watery discharge, rapidly becomes purulent, conjunctival hyperemia and chemosis. Infection is usually bilateral. Untreated infection can lead to keratitis, corneal perforation and blindness. Diagnosis by gram stain and culture of the secretions. Treatment of local infection by single IM dose of ceftriaxone with irrigation of eye with saline solutions at frequent intervals. Disseminated disease treated with 7 days course of ceftriaxone or cefotaxime. Topical erythromycin drops is recommended for all newborn to prevent gonococcal ophthalmia.


Chlamydia trachomatis: Infection spread from maternal genital tract to the newborn, the nasopharynx is the most common site of infection. There is ocular congestion, edema, and discharge developing 5-14 days. Treatment of infants with conjunctivitis and pneumonia with oral erythromycin, 50mg/kg for 14 days. Topical treatment of conjunctivitis is ineffective.


Systemic infections Sepsis and meningitis: Both are difficult to be separated and usually occur together. Risk factors for developing meningitis and sepsis: Prematurity. LBW infants, their own IgG response to infection is reduced. Neonatal neutrophil ingest and kills bacteria less effectively than adult neutrophils. Premature rupture of membranes. Specific instrumentations ( endotracheal intubation, IV cannula, and umbilical catheterization). Male sex.


Early onset sepsis: the onset is from birth to the 7th day of life. 85% presented within the first 24hr, smaller percentage of patients present between 48 hours and 6 days of life. The causative organisms are bacteria that present in the maternal genital tract, like group B streptococcus, E.coli, Klebsiella, listeria monocytogens, and non typable Hemophilus influenzae. Pneumonia is more common in early onset sepsis, whereas meningitis and bacteremia are more common in late-onset sepsis.

Clinically infants had tachypnea, grunting, cyanosis, poor feeding, lethargy, pallor, jaundice, hypothermia, bulging fontanel or convulsion, abdominal distension, diarhhea. Skin mottling, sclerema Also may be presented with shock, meningitis, DIC, acute tubular necrosis. Investigations should include full septic screen: Blood and CSF cultures, urine, stool cultures, umbilical swab for culture. Normal CSF of newborn show protein content of 100-150mg/dl, WBC 25-30 cells mostly lymphocytes in the absence of infection.

Complete blood count may show neutropenia, and thrombocytopenia. Positive c-reactive protein. CXR may show pneumonia. Treatment by combination of ampicillin and gentamicin until the result of culture and sensitivity. Or combination of ampicillin and cefotaxime. Dose: ampicillin 200mg/kg divided 12 hourly, cefotaxime 100mg/kg divided 12 hourly, gentamicin 4mg/kg single daily dose. Duration of treatment for 14 days, and if meningitis present, duration may be extended to 21days. Additional therapy may include, granulocyte transfusion, and intravenous immunoglobulin.


Late onset sepsis: Occurs from 8-90 days after birth. Usually occurs in infant who is recently discharged from newborn nursery. It is acquired from the care giving environment. Clinically the infant is lethargic, had poor feeding, hypotonia, seizures, bulging anterior fontanel, and jaundice. Organisms involved include: coagulase-negative staphylococci, Staphylococcus aureus, E coli, Klebsiella, Pseudomonas, Enterobacter, Candida, GBS. Meningitis occurs in 75% of cases, osteomyelitis( staph. Aureus, group B strep.) or septic arthritis( gonococcus, staph. Aureus), or urinary tract infection. Antibiotic used here should cover resistant microorganisms e.g.vancomycin, third generation cephalosporin.

Note: in the intestine some of conjugated bilirubin will be deconjugated to indirect bilirubin by the effect of glucuronidase



Factors that increase the level of indirect bilirubin in the neonate: Any hemolytic disease that increase level of indirect bilirubin. Any compound compete with bilirubin binding sites to albumin, will displace bilirubin from albumin. Example, free fatty acids and sulfisoxazole. Decrease concentration of glucuronyl transferase enzyme in preterm infant and in cases of hypoglycemia. Any conditions that increase enterohepatic circulation will increase indirect bilirubin, like delayed passage of meconium.

Causes of indirect hyperbilirubinemia: Physiological jaundice: It is a common cause of jaundice in most newborns during the first week of life. Causes: Increased RBC volume, RBC destruction Defective hepatic uptake of bilirubin from blood Defective bilirubin conjugation( immaturity of glucuronyl transferase enzyme)


Type of bilirubin is indirect. The baby looks healthy, feeding well, no organomegaly. It rarely requires phototherapy. Serum bilirubin level is slightly higher among breast fed babies. The onset is from the second day of life, reaches a peak level of no more than 12mg/dl on day 3-5(full term), in preterm peak level may reach 15mg/dl Then bilirubin level gradually declining until 7th-10th day of life.


Causes of Pathological Jaundice: A/Increased production 1.Fetomaternal blood group incompatibility: Rh, ABO 2.Hereditary spherocytosis. 3 Enzyme defect: G6PD deficiebcy, pyruvate kinase deficiency. 4.Sepsis. 5.Increased enterohepatic circulation: Pyloric stenosis, or large bowel obstruction. B/Decreased clearance 1.Congenital: Criggler-Najjar syndrome. 2.Drugs and Hormones: Hypothyroidism, breast milk jaundice.

Neonatal jaundice

Unconjugated
Conjugated
Hepatic
Post-hepatic
Pathologic
Physiologic
Non hemolytic
Hemolytic
Extrinsic
Intrinsic


Intrinsic causes of hemolysis Membrane conditions Spherocytosis Hereditary elliptocytosis 2. Systemic conditions Sepsis 3. Enzyme conditions Glucose-6-phosphate dehydrogenase deficiency Pyruvate kinase deficiency

Extrinsic causes of hemolysis: ABO and Rh isoimmunization. Non-hemolytic causes Cephalohematoma Polycythemia Sepsis Hypothyroidism Gilbert's syndrome Crigler-Najjar syndrome

Hepatic causes( conjugated) Clinically the newborn will have a yellow-green skin color, passing dark urine and pale stool 1. Infections Sepsis Hepatitis B TORCH infections 2. Metabolic Galactosemia Alpha-1-antitrypsin deficiency Cystic fibrosis 3. Idiopathic

Post-hepatic Biliary atresia( extrahepatic or intrahepatic) choledochal cyst

Investigations
Of Unconjugated hyperbilirubinemia: Total s.bilirubin: direct and indirect Coombs test( positive in Rh and ABO incompatibility) 3. Complete blood count and blood film ( spherocytes) 4. Retic count: increased with hemolysis.
Of conjugated hyperbilirubinemia: Liver enzyme level(SGPT, SGOT) Bacterial and viral culture. TORCH screen Hepatic ultrasound, CT scan. Metabolic screen Sweat chloride test Liver biopsy

Breast milk jaundice: Characterized by unconjugated hyperbilirubinemia without evidence of hemolysis during the 1st-2nd week of life. Breast milk may contain inhibitors of glucuronyl transferase enzyme, or it may increase entero-hepatic circulation of bilirubin by the effect of breast milk glucuronidase. Bilirubin rarely reaches a dangerous level, and does not need exchange transfusion. The baby is healthy, growing well and there is no hepatosplenomegaly or anemia. Interruption of breast feeding for 1-2 days result in rapid decline of bilirubin. It may persist for 3-4 weeks, there is no need to stop breast feeding.

Crigler Najjar syndrome: It is a form of indirect hyperbilirubinemia in which there is defective conjugation of bilirubin due to permanent deficiency of glucuronyl transferase enzyme. Inherited as AD,AR. Infants usually require frequent exchange transfusion and remain on phototherapy for prolonged period of time. Gilbert syndrome: Indirect hyperbilirubinemia due to defect in hepatic uptake of unconjugated bilirubin.

Differential diagnosis of prolonged neonatal jaundice: Neonatal jaundice may persist for >2 weeks after birth. Breast milk jaundice Sepsis Biliary atresia Hepatitis TORCH infection Galactosemia Hypothyroidism Congenital spherocytosis G6PD deficiency.


Kernicterus: It is a neurologic syndrome resulting from deposition of unconjugated bilirubin in the brain cells( basal ganglia), characterized by: Early manifestations: Lethargy, hypotonia, irritability, weak moro reflex, poor feeding, and high pitched cry. Late manifestations( more than 1st week): Opisthotonic posture( neck retraction), hypertonia, seizures By the end of the first year, the infant will have nerve deafness, chorioathetoid cerebral palsy, developmental delay, mental retardation.


The free indirect bilirubin( not bound to albumin) will cross the blood-brain barrier because of its lipid solubility, or because of disruption of BBB under the effects of asphyxia, acidosis, and sepsis, and in turn will be deposited in the basal ganglia. In full term infants kernicterus rarely occur at S.bilirubin level below 20mg/dl, while in preterm infants, kernicterus may occur at lower levels. Factors that increase risk of kernicterus even at low S.bilirubin level: Sepsis, meningitis, hemolysis, hypothermia, asphyxia, hypoglycemia, prematurity, and drugs that displace birubin from its binding sites like sulfa drugs and ceftriaxone. Prevention: by early initiation of phototherapy or exchange transfusion, treating above risk factors.


Treatment of hyperbilirubinemia: Phototherapy: It reduces the indirect bilirubin level. It works through a process of photo-isomerization that changes the bilirubin into water-soluble isomers that can be passed without getting stuck in the liver. Blue or white lights are effective with 425-475nm wavelength. It is indicated in full term newborn without risk factors, at S.bilirubin level of 16-18mg/dl, and a lower level in preterm babies(12-15mg/dl) according to body weight. Newborn eyes should be covered to avoid light toxicity.


It requires 6-12hr to have a measurable effect. It reduces S.bilirubin level by 1-3mg/dl/12-24hr The newborn should be placed about 15-20 cm from the fluorescent lamp. Complications of phototherapy: Increased insensible water loss and dehydration. Diarrhea with green stool. Maculopapular skin rash. Lethargy. Risk of retinal damage. Skin may turn bronze color if the newborn have direct hyperbilirubinemia


Exchange transfusion: it is indicated when there is a high level of indirect bilirubin at risk of kernicterus. It is effective in removing sensitized RBC before they are hemolysed, also removes 60% of bilirubin from plasma. It is indicated in a full term newborn with s.bilirubin level of 20mg/dl with evidence of hemolysis, and without evidence of hemolysis at a level of 25mg/dl(weight>2000g). In preterm baby it is indicated at a lower bilirubin level,and calculated as 1% of body weight in gram Example: 1500g exchange level 15mg/dl 1200g exchange level 12mg/dl N.B if there is risk factors exchange should be done at a lower bilirubin level.

The blood prepared for exchange should be whole blood, fresh, And cross-matched with the mother and baby. The total amount of blood exchanged equal to twice the baby blood volume: Amount of blood=infant weight(kg)x85mlx2 10-20 ml of blood is withdrawn and infused per cycle The whole process last about 45-90min For each 100ml of blood exchanged, we give 1 ml calcium gluconate. Exchange transfusion is done through umbilical venous catheter.


Complications of exchange transfusion: Transfusion reaction( incompatibility of blood). Hyperkalemia( specially when old blood is used) Hypocalcaemia Infection(sepsis from catheterization, or blood borne infection like hepatitis) Vessel perforation, hemorrhage, or thrombosis. Hypotension Necrotizing enterocolitis.

Rh isoimmunization:Rh antigens are C,D,E,c,and e. here usually mother has Rh –ve blood group and the baby is Rh+ve.When small quantities( 30ml) of Rh+ve fetal blood containing D antigen enters maternal circulation( during abortion or at time of delivery), antibodies against fetal antigen will be produced in unsensitized mother.These maternal antibodies will readily cross the placenta, causing hemolytic disease of fetus or newborn.Hemolytic disease rarely occur in the first born baby, because transfusion of fetal RBC into maternal circulation tend to occur at time of delivery.

When the mother and her fetus are also incompatible with respect to A or B, there is less chance of maternal sensitization because of rapid clearance of fetal cells by her antiA or antiB antibodies which are IgM that doesn't cross the placenta. There is a tendency for the severity of Rh disease to worsen with successive pregnancies. Clinical manifestations: A wide spectrum of hemolytic disease occur in affected infant: Hydrops fetalis: here there is severe sensitization in utero, the newborn have severe anemia, signs of respiratory distress, cardiomegaly, HF, hepatosplenomegaly, severe edema, and may die shortly after birth. jaundice is usually absent at birth because of placental clearance of lipid soluble unconjugated bilirubin.



In moderate sensitization, baby born with pallor, jaundice in the first few hours of birth, hepatosplenomegaly. In mild hemolysis(15%), the baby may have only mild anemia and jaundice that may require blood transfusion only with phototherapy. Laboratory findings: ABO and Rh blood group for mother and newborn Direct coombs test is positive. Anemia, Hb may reach 3-4g/dl Increase retic count. Cord bilirubin may be 3-5mg/dl, and raise rapidly to high level during first 6 hours.


Antenatal diagnosis and management: If mother is sensitized, then send for RhD(IgG) antibody titer at 12-16 weeks of gestation, and at 36 weeks. If the titer is rapidly increasing or 1:64, means significant hemolysis. The antibodies are monitored and if levels increase, amniocentesis, fetal umbilical cord blood sampling, and ultrasound are used to assess any effects on the baby. If the baby is in danger, and the pregnancy is at least 32-34 weeks, labor is induced. Under 32 weeks, the baby is given blood transfusions while still in the mother's uterus.

ABO incompatibility:Usually the mother is type O blood group and the newborn is A or B blood group( mothers with blood group A or B, sensitization will not occur because the have IgM antibodies which doesn’t cross the placenta)Because many mothers with O blood group already have IgG antibodies against A and B before pregnancy, so the first born infant will be affected.Clinically the newborn will have jaundice and pallor in the first day of lifeHydrops fetalis is extremely rare.Hemolysis usually is less severe and its severity decline with successive pregnancies.

Investigations: Direct coombs test is weakly positive. Blood smear show spherocytes. Increase indirect bilirubin. Hb may be normal or 10gldl. Retic count is increased. Treatment: Phototherapy, and if serum bilirubin level reaches a high level, exchange transfusion should be done with fresh whole blood( blood group of mother and Rh of baby). Blood transfusion in case of anemia only.


Infant of diabetic mother: Control of DM with insulin has lead to improved outcomes in diabetic pregnant mother. Diabetic mothers have a high incidence of polyhydramnios, preeclampsia, pyelonephritis, preterm labor, and chronic hypertension. Most infants of diabetic mothers are large for gestational age( macrosomic), but if diabetes complicated by vascular disease, infant may be growth restricted. The neonatal mortality rate is 5 time that of infants of non-diabetic mother.

Pathophysiology: Maternal hyperglycemia causes fetal hyperglycemia, the fetal pancreatic response leads to fetal hyperinsulinemia. Fetal hyperinsulinemia and hyperglycemia will cause increase hepatic glucose uptake and glycogen synthesis, accelerated lipogenesis and augmented protein synthesis. The related pathologic findings are hypertrophy and hyperplasia of pancreatic islets, increased weight of placenta and infant organs.


Then separation of placenta at birth suddenly interrupts glucose infusion to the neonate without proportional effect on hyperinsulinism, so hypoglycemia will develop immediately after birth. Cortisol and growth hormone levels are normal. Congenital anomalies correlates with poor metabolic control during organogenesis period and may be due to hyperglycemia induced teratogenesis.

Clinical manifestations: Infants born to mothers with glucose intolerance are at an increased risk of morbidity and mortality related to the following: Respiratory distress (due to antagonistic effect of insulin on stimulation of surfactant synthesis by cortisol). Growth abnormalities large for gestational age, plump(more than 4kg) as a result of increased body fat and enlarged viscera, with puffy plethoric face, so may be complicated by shoulder dystocia during labor, brachial plexus injury. or the newborn may be small for gestational age 20%

Hypoglycemia :

in 20-25% of infants, the nadir in infant blood glucose level is usually reached between 1-3 hours. The infant tend to be jittery, tremulous and hyper excitable, convulsion may occur during the first three days of life, although hypotonia, lethargy and poor sucking may occur.

4. Hyperviscosity secondary to polycythemia (may lead to hyperbilirubinemia) Hypocalcemia, hypomagnesaemia, and iron abnormalities Congenital malformations: A. congenital heart disease(cardiomegaly in 30% of cases, VSD,TGA, truncus arteriosus and coarctation of aorta). B. Neural tube defects, hydronephrosis, renal agenesis, duodenal atresia, situs inversus, and small left colon syndrome.

Prognosis: There is subsequent increased incidence of DM in infants of diabetic mother in comparison to that of general population. Physical development is normal but they are predisposed to childhood obesity. Treatment: During pregnancy: frequent evaluations of all pregnant mothers with overt gestational DM by evaluation of fetal maturity and to plan the delivery of these infants in the hospitals where expert obstetric and pediatric care is available.

Workup RBS: blood glucose measurements as soon as possible after birth, within 2-3 hours after birth and before feeding, and at any time abnormal clinical signs are observed. CBC: polycythemia, PCV 65% or more. Serum Magnesium level. Serum calcium. TSB Arterial blood gas analysis. CXR: cardiomegaly, RDS.

Postnatal: Asymptomatic infants should have a blood glucose determination within 30 min of birth and then every hour in the next 6-8hr, if he is well with normoglycemia, then start oral feeding as soon as possible and continued at 3 hr interval. Serum or blood glucose levels < 20-40 mg/dL within the first 24 hours after birth are generally agreed to be abnormal and require intervention. if blood glucose does not increase after feeding, or if the infant develops symptoms of hypoglycemia, then give intravenous 10% glucose 200mg/kg( 2 ml/kg) within 5-10 min, then infusion at a rate of 4-8 mg/kg/min. Target blood glucose level is more than 45 mg/dl.


If hypoglycemia recurs, increase dose of glucose by 2mg/kg/min. Bolus injection of hypertonic glucose should be avoided because it may aggravate hyperinsulinemia and cause rebound hypoglycemia. If hypoglycemia continues, hydrocortisone may be given or diazoxide. Once the infant's glucose levels have been stable for 12 hours, IV glucose may be tapered by 1-2 mg/kg/min, depending on maintenance of preprandial glucose levels higher than 40 mg/dL. Correct metabolic problems like hypocalcemia, hypomagnesemia. Treatment of RDS.

Clinical types of neonatal seizure:

Clinical sign
Seizure type
Eye deviation, Blinking, fixed stare Repetitive mouth and tongue movements Apnea Pedaling, tonic posturing of limbs
1-Subtle (common)
May be focal or generalized Tonic extension or flexion of limbs (often signals Severe ICH in preterm infants)
2-Tonic
May be focal or multifocal Clonic( jerky) limb movements (synchronous or asynchronous, localized or often with no anatomic order to progression) Consciousness may be preserved Often signals focal cerebral injury.
3-Clonic
Rare, Focal, Multifocal, or Generalized Lightning-like jerks of extremities (upper>lower)
4-Myoclonic


Differentiation of Seizures from Nonconvulsive Movements:-Jitteriness is distinguished clinically from clonic seizures byno associated ocular movements or autonomic phenomena,stimulus sensitivity.tremor that is suppressed by flexing the limb.Distinguish benign neonatal sleep myoclonus (occurs in healthy newborns) from myoclonic seizures.-EEG monitoring and video display in newborns with subtle seizures and generalized tonic seizures has not shown consistent electrographical discharges. -Some of these movements may be brainstem release phenomena rather" epileptic seizures”.

MAJOR CAUSES OF NEONATAL SEIZURES: Several causes often coexist! onset1-Hypoxic-ischemic encephalopathy <3 days 2-Metabolic: Hypoglycemia <2 days Hypocalcaemia Early-onset 2–3 days Late-onset >7 days Hypomagnesaemia (often with Hypocalcaemia) Hyper/Hyponatremia Drug Withdrawal <3 days Local Anesthetic Toxicity Pyridoxine (Vitamin B6) Dependency Disorders of Small Molecules (Amino Acid, Organic Acid &Urea Cycle Disorders)

3-Intracranial infection <3 days Bacterial meningitis (E. coli, Group B Strep, Listeria) Viral Encephalitis (Herpes Simplex, Enterovirus) 4-Intrauterine Infection (CMV, Toxoplasm., HIV, Rubella, Syphilis ) >3 days 5-Cerebral Vascular Intraventricular hemorrhage <3 days Primary subarachnoid bleed <1 day Subdural/epidural hematoma Focal Ischemic Necrosis (Stroke) Variable

6-Developmental defects Variable Neurocutaneous Disorders (Tuberous Sclerosis) 7-Epilepsy Syndromes Epileptic Encephalopathies Benign Familial Neonatal Convulsions Diagnostic evaluation: 1-Metabolic screen: blood glucose level, calcium, magnesium level 2-Complete blood count, CSF examination in case of sepsis or meningitis. 3- Screening for TORCH infection when suspected.

4-ELECTROENCEPHALOGRAPHY (EEG) Is essential in diagnosis and management of neonatal seizures. As there may not be ictal activity on EEG even during a seizure (electroclinical dissociation), serial EEGs or continuous EEG monitoring are of benefit. 5- NEUROIMAGING: Imaging the brain is essential in determining the etiology of neonatal seizures. In the acute setting, after control of the seizures, MRI scanning is very effective for determining the presence and extent of hypoxic-ischemic injury and of parenchymal brain injury. If MRI scanning is not possible acutely, CT scan is effective for determining the presence of hemorrhage and calcification( e.g., congenital infection, cortical dysplasia).

MANAGEMENT: Neonatal seizures require urgent treatment to prevent brain injury. Give anticonvulsant medication only after adequate ventilation and perfusion have been established and the blood glucose concentration has been measured. 1. Ensure adequate ventilation and perfusion. 2. Correct metabolic disturbances. Hypoglycemia: (10% glucose in water) 2 mL/kg IV (0.2 g/kg) as bolus. Follow with continuous infusion at up to 8 mg/kg/min IV Hypocalcemia: (calcium gluconate 10%) 100mg/kg IV over 1 to 3 minutes (Note: Monitor cardiac rhythm for bradycardia) Follow with maintenance of 500 mg/kg/24 hrs IV or PO Hypomagnesemia: (magnesium sulfate) 25-250 mg/kg/dose IV/IM


3. Begin anticonvulsant therapy. Start with diazepam 0.1-0.3mg/kg/dose slow IV injection to avoid respiratory suppression and apnea. If seizure recurrent give: Phenobarbital: 20 mg/kg IV loading dose (Note: monitor respiration) Maintenance: 5 mg/kg/24 hrs IV/PO divided 12 hourly Before giving second dose or second medication ask yourself: (1) Do I have the correct diagnosis? (2) Are ventilation and perfusion optimal? (3) Have I recognized and corrected any metabolic disturbance? Then if seizure still not controlled, phenytoin can be given by infusion in 0.9% NaCl ( same dose of phenobarbital)


Lorazepam: 0.05 mg/kg to 0.10 mg/kg IV over several minutes. (Note: Monitor closely for respiratory depression.) duration of action 6-24 hours. Trial of pyridoxine if refractory seizures in a single dose of 100mg/kg. DURATION OF TREATMENT: The following guidelines aim to continue Phenobarbital for the briefest time possible: When seizures have stopped and if the neurological examination is normal, consider stopping Phenobarbital. If the neurological examination remains abnormal, then consider stopping medication if the EEG is normal

Prognosis( outcome): The outcome following neonatal seizures depends primarily on the underlying cause. The presence of both clinical and electrographic seizures in the newborn often indicates some degree of brain injury. Those with some degree of brain injury often go on to develop epilepsy, developmental delay, and cerebral palsy Prognosis is bad if asphyxia as cause.

Hemorrhagic Disease of Newborn: It is a term describes a bleeding disorder in the newborn baby that is due to vitamin K deficiency. Coagulation factors II, VII, IX, and X depend on the presence of vitamin K for their activity. vitamin K deficiency bleeding is usually classified by 3 distinct time periods after birth, as follows: Early-onset vitamin K deficiency bleeding in the newborn usually occurs during the first 24 hours after birth. It is seen in infants born to mothers taking anticonvulsant or antituberculosis medication.


2. Classic vitamin K deficiency bleeding in the newborn which usually occurs after 24 hours and as late as the first week of life it is observed in infants who have not received prophylactic vitamin K at birth. The incidence ranges from 0.25-1.7 cases per 100 births. Bleeding commonly occurs in the umbilicus, GI tract (melena), skin, nose, surgical sites (circumcision), and, uncommonly, in the brain.

3. Late-onset vitamin K deficiency bleeding in the newborn: This usually occurs between age 2-12 weeks; however, late-onset vitamin K deficiency bleeding can be seen as long as 6 months after birth. This disease is most common in breastfed infants who did not receive vitamin K prophylaxis at birth. More than half of these infants present with acute intracranial hemorrhages.

Differential diagnosis: Consumption coagulopathy Von Willebrand disease Maternal isoimmune thrombocytopeniaAlloimmune thrombocytopenia Hepatobiliary disease Investigations: Prolonged prothrombin time( PT) is important in the diagnosis. Platelet counts and fibrinogen levels within the normal range for newborns. Thrombocytopenia or a prolonged aPTT should prompt workup for other causes of bleeding during the neonatal period. The diagnosis of vitamin K deficiency bleeding is confirmed if administration of vitamin K halts the bleeding and reduces the PT value.

Prevention: With intramuscular vitamin K in a single dose(1 mg for full term and 0.5 mg for premature) after birth effectively prevents classic vitamin K deficiency bleeding. Treatment: Because the bleeding in classic vitamin K deficiency bleeding usually is not life threatening, a single dose of parenteral vitamin K (subcut. Injection) is sufficient to stop the bleeding and return prothrombin time (PT) values to the reference range. IM administration can result in a hematoma because of the coagulopathy. Intravenous (IV) administration of vitamin K has been associated with anaphylactoid like reactions.

Fresh frozen plasma may be considered for moderate-to-severe bleeding. Life-threatening bleeding may also be treated with prothrombin complex concentrates. Complications of treatment include anaphylactoidlike reactions during intravenous (IV) vitamin K administration, hyperbilirubinemia or hemolytic anemia after high doses of vitamin K, and hematomas at the site of injection, if administered IM. The best sources of vitamin K are green leafy vegetables, legumes, soybean and olive oils.