Module 3. Neonatology.

Lesson 6.

Topics:

Theme 1. Asphyxia of newborns. Etiology. Pathogenesis. Classification Clinic. Diagnostics. Differential diagnosis. Neonatal resuscitation. Treatment. Prevention. Outlook.

Theme 2. Birth trauma. Etiology. Pathogenesis. Classification. Clinic. Diagnostics. Differential diagnosis. Treatment. Prevention. Outlook.

 

An introduction to the neonatology.  Medical care for the newborns in a maternity hospital.

Neonatology is a part of pediatrics which studies newborn infant, its physiology, and pathology; treatment, and prevention of its diseases, and disorders; peculiarities of nursing, and feeding.

Neonatological terms

Gestational age (or more correctly the menstrual age) is measured from the first day of the mother’s last normal menstrual period. The average gestational age is 40 weeks (280 days). The majority of infants are born between 37 weeks (259 days) and 42 weeks (294 days) and are referred to as term infants.  Preterm infants are those born before 37 weeks while post-term infants are born on or after 42 weeks.  Infants are no longer described as premature or post-mature.

Intrauterine periods of development:

1.                 Embrional development begins from the zygote formation, lasts till 8 weeks of gestation. In this period different organs and systems are formatted. Risk factors: genetical, physical, chemical, alimentary, toxicosis, mother’s diseases.

2.                 Placental development begins in the 8 weeks of gestations. Continue till the end of pregnancy. Is characterized by differentiations of fetal tissues and organs, enlargement of the fetus weight and length.

Risk factors: external influence, mother’s diseases, toxemia, immune incompatibility between mother and fetus, placental disorders, placental placement and development abnormalities, umbilical cord and fetal membranes abnormalities.

Intranatal, neonatal and perinatal periods:

Intranatal period begins from the first signs of the delivery, extends until the birth of the baby. Risk factors: delivery abnormalities, intra birth infection of the newborn.

Neonatal period begins from the birth of the baby, extends until 28 days after birth. Neonatal period divides on:

1.                 Early neonatal period – from the birth until 7 days after birth.

2.                 Late neonatal period – from 7 days until 28 days after birth.

Perinatal period begins from 28 weeks of gestation, extends until the 7 days after delivery, and includes:

a) late antenatal period (from 28 weeks of gestation to 40 weeks of gestation);

b) intranatal period (from the first signs of the delivery until the baby is born);

c) early neonatal period (from the birth of the baby until 7 days after birth)

Live birth – the complete expulsion or extraction from its mother of a product of conception, irrespective of the duration of the pregnancy, which, after such separation, breathes or shows any other evidence of life such as heartbeat, umbilical cord pulsation, or definite movement of voluntary muscles, whether the umbilical cord has been cut or the placenta is attached. A live birth is not necessarily a viable birth. See early neonatal death.

THE INFANT AT BIRTH

Apgar score: The normal neonate should breathe and cry within 30 seconds.  The following procedure is followed immediately after the baby is born. This should be done at one minute and usually is repeated at five minutes. Scoring system designed by Virginia Apgar ca. 1953 for heart rate, respiratory effort, tone, reactivity, color. By convention, scores are assigned at 1 and 5 minutes, with additional scores given at 5-minute intervals if the most recent score is less than 7. The 1 minute score indicates the need for resuscitation, while the 5 minute score gives an indication of the success of the resuscitation attempts.  

However, if the one-minute score is normal the assessment at five minutes is ofteot required.

Clearing the airway Suctioning the mouth and pharynx is usually unnecessary if the infant cries well at birth and the one minute Apgar score is normal.  Suctioning with a soft catheter and low negative pressure not exceeding -10 cm H20 may be required to clear blood or excessive mucus in selected cases (e.g. after Caesarian section).  Suctioning should be gentle and as brief as possible to avoid reflex apnea, bradycardia or damage to the mucous membranes.

Heat conservation Measures should be taken to prevent excessive cooling of the infant e.g. early drying, warm towel, warm delivery room, prevention of unnecessary exposure, etc.  Too often the baby is left exposed in a cold draughty labor ward and forgotten, while the attendant concentrates on the mother.

Umbilical cord   In the normal infant the umbilical arteries go into spasm at delivery.  It is advisable to delay clamping the cord until the baby has taken a few breaths so as to encourage transfusion of blood via the umbilical vein into the infant’s circulation from the placenta.  There is, however, no difference in the hemoglobin concentration at three months between babies with early or late clamping of the umbilical cord.

Immediate clamping of the cord is indicated in asphyxiated babies (who need resuscitation) or in cases where Rhesus incompatibility is expected.

A sterile plastic umbilical clamp or tie is applied around the cord 2 cm from the skin and the cord above this is cut off.  Subsequent care entails application of 90% alcohol (surgical spirits) to the stump twice a day.  The stump will usually come away between 7-10 days after birth.

Eyes  Routine prophylaxis against Gonococcal ophthalmia neonatorum is recommended.  Chloromycetin eye ointment is usually used or 20 % natrii sulfacyl.  Erythromycin or tetracycline has the added advantage of activity against Chlamydia infection.

Vitamin K₁ Each newborn should receive an intramuscular injection (into the anterolateral thigh) of 1 mg vitamin K1 to prevent hemorrhagic disease of the newborn.

Position of the baby after birth Although it is often suggested that the baby be laid in a 10^o head down position, there is no evidence that this has any benefit over being placed flat on his/her side.

The initial assessment of the newborn Immediately after birth the baby is briefly examined to exclude:

·                   birth trauma e.g. facial palsy, fractures

·                   congenital deformities e.g. meningomyelocoele, club foot, exomphalos, anal atresia, genital anomalies, etc.

·                   respiratory distress

·                   severe anaemia

Maternal Handling If circumstances permit, the mother should be encouraged not only to hold but also to suckle her baby immediately after delivery.  This is not only of psychological benefit but also stimulates uterine contractions which fascilitate delivery of the placenta.  The sucking reflex is at its height after birth.

Further care of the baby The baby should be weighed and the head circumference measured.  Length usually is not recorded as it is difficult to measure accurately.  If there is any doubt about the well-being of the baby, observe the newborn infant for a few hours in a nursery before he/she goes to the mother (the healthy infant delivered by Caesarian section is usually observed for a few hours only).  This period provides an ideal opportunity to look out for hypothermia, respiratory distress, abnormal neurological features such as jitteriness, convulsions, excessive lethargy, etc.  Normal term infants delivered vaginally should remain with their mothers.

The first bath A normal baby may be bathed on the first day provided his temperature is within the normal range (i.e. approximately 36^oC).  Early bathing is of no physiological advantage to the baby and should certainly be delayed in ill infants.  Infants born to HIV positive women are often bathed after delivery to remove contaminated blood and secretions.

The first feed The normal infant should be put to the breast immediately after birth.  This prevents hypoglycemia, allows assessment of sucking ability and provides antibodies in the colostrum.  If not put to the breast at birth, let the infant suckle as soon as possible.

Later feeding of the newborn is 7 times a day every 3 hours with a night 6-hour break. Milk volume could be found by formula: 2% body weight * N (number of days of life). This is all day volume. If drinking is need it is calculated as 5ml * body weight * day of life per day. 5% glucose or boiled water could be given.

Delivery Room Examination The purpose of the delivery room history and examination is to identify major congenital malformations or other risk factors that would mandate transfer to the Neonatal Intensive Care Unit rather than the Newborn Nursery.

History: Inquire about high risk factors which may be assoclated with respiratory depression, such as: antepartum fetal bradycardia or tachycardia, meconium-stained amniotic fluid, maternal fever, placental abnormalities, premature or prolonged rupture of membranes (PROM), administration of narcotics, preeclampsia or eclampsia, diabetes, multiparity, use of recreational drugs, abnormal presentation of the fetus.

Physical Examination:

General	Petichiae, rash, evidence of birth trauma, lacerations, jaundice? Weight <1800 gm?
Fontanelle	Bulging, depressed, anterior fontanelle abnormally large (>2×2 cm), posterior fontanelle open?
HEENT	Caput succadaneum? (Soft, ill defined in outline, represents edema of the scalp e.g. often seen after suction extraction) Cephalhematoma? (Doesn’t cross suture lines, usually appears on 2nd day of life.) Eyes? Ears normally positioned? Nares patent? Cleft lip or palate? Neck masses? NG tube passes OK?
Chest	Breath sounds equal? Good air entry? Presence of stridor, wheezing, flaring, retracting, grunting, cyanosis in room air?
CVS	Rate >120 and regular? Murmers? Normal PMI? Femoral pulses easily palpated?
Abdomen	Masses? Size of liver and spleen below mid-costal margin? Distension? Scaphoid? 3-vessel cord?
GU	If male, testes descended bilaterally? Inguinal masses? Hypospadias? If female, bulging hymen (imperforate)?
Back	Midline defects? Anus patent?
Neuro	Alertness? Tone? Symmetric movement? (Erbs Palsy: lack of movement in one arm.) Facial palsy? Moro, grasp, suck, cry, Babinski? Evidence of neural tube abnormalities?

Detailed Newborn Examination

General Measure and record height, weight, and head circumference. If the infant appears premature or is unusually large or small, perform a Dubowitz/Ballard exam to assess gestational age (see Dubowitz/Ballard scoring grid). The exam is divided into two parts: an external characteristics score, which is best done at birth, and a neuromuscular score, which should be done within 24 hours after birth.

Skin Color

·                   Pallor – associated with low hemoglobin

·                   Cyanosis – associated with hypoxemia

·                   Plethora – associated with polycythemia

·                   Jaundice – Elevated bilirubin

·                   Slate grey colour – associated with methemoglobinemia

Skin Lesions Milia, miliaria; erythema toxicum; cafe au lait spots – suspect neurofibromatosis if there are many large spots. Junctional nevi – if large numbers, suspect tuberous sclerosis, xeroderma pigmentosus, generalized neurofibromatosis.

Neurological Exam

State of alertness Check for persistent lethargy or irritability.

Posture In term infant, normal position is one with hips abducted and partially flexed and with knees flexed. Arms are adducted and flexed at the elbow. The fists are often clenched, with fingers covering the thumb.

Tone Support the infant with one hand under his chest. The neck extensors should be able to hold the head in line for 3 seconds. Should not have more than 10% head lag when moving from supine to sitting position.

Reflexes Reflexes must be symmetrical. Biceps jerk test C5 and C6, Knee jerk tests L2-L4, Ankle jerk tests S1, S2. Truncal incurvation reflex tests T2 through S1. Anal wink test S4, S5. Other primitive reflexes include the Moro, palmer and planter grasps, sucking and rooting reflexes, and the asymmetric tonic neck reflex (ATNR). Asymmetric tonic neck reflex (seen in ventral suspension with arms rigidly extended and fists clenched) is abnormal.

When reflexes appear and disappear:

Reflex	Appears	Disappears
Moro	Newborn	3 months
Grasp	Newborn	3 months
LE crossed extensors	Birth	1 month
Extensor plantar	Newborn	8-12 months
Placing/stepping	Birth	1-2 months
ATNR	Newborn	3 months

Head and Neck

Head Check for overriding sutures, the number of fontanelles and their size. Check for abnormal shape of head. Check for encephalocoeles. Measure the head circumference.

Eyes Check for colobomas, heterochromia.

·                   Cornea – Check for cloudiness.

·                   Conjunctiva – Inspect for erythema, exudate, edema, jaundice and hemorrhage. Silver nitrate prophylaxis can cause a chemical conjunctivitis. Check for pupillary size and reactivity to light.

·                   Red Reflex – Hold the ophthalmoscope 6-8″ from the eye. Use the +10 diopter lens. The normal newborn transmits a clear red colour back to the observer. Black dots may represent cataracts. A whitish color may be suggestive of retinoblastoma.

Ears Check for asymmetry, irregular shapes. Look for auricular or pre-auricular pits, fleshy appendages, lipomas, or skin tags.

Nose Look for flaring of the alae nasi as a sign of increased respiratory effort. Look for hyper- or hypo-telorism. Check for choanal atresia (CA) as manifested by respiratory distress (neonates are obligate nose breathers). A soft NG tube should be passed through each nostril to confirm patency if choanal atresia is suspected.

Palate Check for cleft lip and palate.

Mouth Observe the size and shape of the mouth.

·                   Microstomia – seen in Trisomy 18 and 21.

·                   Macrostomia – seen in mucopolysaccharidoses.

·                   Fish mouth – seen in fetal alcohol syndrome.

·                   Epstein pearls – small white cysts which contain keratin, frequently found on either side of the median raphe of the palate.

·                   Ranulas – small bluish white swellings of variable size on the floor of the mouth representing benign mucous gland retention cysts.

Tongue Macroglossia – Hypothyroidism, mucopolysaccharidoses

Teeth Natal teeth – occur in 1/2,000 births. Mostly lower incisors. Risk of aspiration if loosely attached.

Chin Micrognathia – occurs with Pierre-Robin syndrome, Treacher-Collins syndrome, Hallerman Streiff syndrome.

Neck Palpate over all muscles, palpate clavicles for possible fractures. Web neck found in Turner’s and Noonan’s syndromes. Torticollis usually secondary to sternocleidomastoid hematoma. Cystic hygromas most commoeck mass. Lymph nodes are unusual at birth and their presence usually indicates congenital infection. Note: Suspect tracheo-esophageal fistula (TEF) if polyhydramnios is present.

Chest and Lungs Observe respiratory rate, respiratory pattern (periodic breathing, periods of true apnea). Observe chest movements for symmetry and for retractions. Listen for stridor, grunting. Note that there may be some enlargement of the breasts secondary to maternal hormones.

Cardiovascular System Measure heart rate, blood pressure in upper and lower extremities, respiratory rate.

Inspection  Check baby’s color for pallor, cyanosis, plethora.

Palpation Check capillary refill. Check pulses; note any decrease in femoral pulses or radio-femoral delay as a sign of possible coarctation of the aorta, note character of pulses (bounding or thready). Locate PMI with single finger on chest; abnormal location of PMI can be clue to pneumothorax, diaphragmatic hernia, situs inversus, or other thoracic problem.

Auscultation Note rhythm and presence of murmurs which may be pathologic.

Abdomen Note shape of abdomen. Flat abdomens signify decreased tone, abdominal contents in chest, or abnormalities in abdominal musculature. Note abdominal distension.

Observe for diastasis recti. Observe for any obvious malformations e.g. omphalocoele. An omphalocoele has a membrane covering (unless it has been ruptured during the delivery) whereas a gastroschisis does not.

Examine umbilical cord and count the vessels. Note color of cord. Palpate liver and spleen. It may be normal for the liver to be about 2 cm below the right costal margin. The spleen is not usually palpable; if the spleen is felt, be alert for congenital infection or extramedullary hematopoeisis. After locating these organs (checking for situs inversus), palpate for any abnormal masses.

·                   Auscultate for bowel sounds.

·                   Examine for hernias – umbilical or inguinal.

·                   Inspect anal area for patency and/or presence of fistulas.

Genitourinary Exam

Kidneys Examined by palpation. The kidneys should be about 4.5-5.0 cm vertical length in the full term newborn. The technique for palpation is either a) one hand with four fingers under the baby’s back, palpation by rolling the thumb over the kidneys, or b) palpate the left kidney by placing the right hand under the left lumbar region and palpating the abdomen with the left hand (do the reverse for the right kidney).

Male genitalia Term normal penis is 3.6±0.7 cm stretched length. Inspect glans, urethral opening, prepuce and shaft. Normally difficult to completely retract foreskin. Observe for hypospadias, epispadias. Inspect circumcised penis for edema, incision, bleeding. Full term infant should have brownish pigmentation and fully rugated scrotum. Palpate the testes.

Female genitalia Inspect the labia, clitoris, urethral opening and external vaginal vault. Often a whitish discharge is present; this is normal, as is a small amount of bleeding, which usually occurs a few days after birth and is secondary to maternal hormone withdrawal. Hymenal tags may be present normally.

Extremities and Skeletal System

Spine Scoliosis, kyphosis, lordosis, spinal defects, meningomyelocoeles.

Upper extremity Look for clavicular fracture, absence of radius or ulna. Inspect creases and fingers.

Lower extremity See posture above. Do Ortolani maneuver to check for congenital hip dislocation. Check toes.

THE HEALTHY NEONATE AND MINOR DISORDERS

Weight
A weight loss of up to 10% of birth weight may occur during the first 3 to 5 days of life. Birth weight is usually regained by the seventh day. Subsequent weight gain is usually about 200g a week (25-30 g/day) for the first three months.

Head and neck

·                      Head circumference – 33 to 37 cm (average 35 cm)

o          Average increase approximately 7.5 mm/week (1 mm a day)

·                     Shape

o         caput succedaneum: oedematous thickening of the scalp in the presenting area.  It disappears within a day or two

o         anterior fontanelle: diamond-shaped and variable size, normally slightly concave and may be seen to pulsate

o         moulding: altered head shape in response to pressure, sometimes with overriding cranial bones

o         plagiocephaly:  “parallelogram skull”, with flattening of one side of the occiput and the opposite frontal region and face.  Distinguish from unilateral craniosynostosis due to premature fusion of one coronal suture with lack of growth on that side (early surgical correctioecessary)

o          craniotabes (softening of skull bones) is a normal finding in most newborns and many infants up to 3 months.

·                    

 

·                     Neck

o          the newborn baby generally appears to have a short neck.  Midline swellings such as dermoid and thyroglossal cysts are uncommon

o         sternomastoid “tumour” – a hard lump in the body of the sternomastoid muscle appearing some days after birth.  Caused by trauma or avascular necrosis.  It may cause torticollis which usually improves with physiotherapy.  Uncommon.

·                     Eyes

o         examination difficult at first because of strong reflex closure.  Baby often opens eyes if held erect.

o         pupil should appear black and not grey.

o          “red reflex” should be present.

o          colour of iris indefinite and not predictable.

o          sclerae often have a blue tinge.

o          tears rare in first few weeks.

o         infants are able to see from birth and should follow a red or bright moving object.

o         subconjunctival haemorrhage:  a bright red patch, often adjacent to the cornea has no serious significance and disappears within a few weeks.

o         abnormally large eye/s may indicate congenital glaucoma (early treatment very important).

·                     Nose and mouth

o         the newborn infant is an obligatory nose breather.  Nasal obstruction, congenital (choanal atresia) or acquired (e.g. nasal secretions), may cause feeding problems or respiratory distress.

o         sucking blisters: thickened areas on the upper lip, usually in the midline.

o         epithelial pearls are small whitish areas a few mm across, usually visible in the midline on the hard palate.  They are of no significance.

o         tongue-tie when the frenulum linguae is inserted into or near the tip of the tongue, rarely interferes with sucking or future speech and is usually best left well alone.

·                     Teeth

o         adventitious teeth may occasionally be present at birth.  They are usually loose, do not interfere with sucking, and fall out spontaneously.  Rarely, primary teeth may also be present at birth.

Skin

·                      Vernix caseosa Protective greasy white substance secreted by fetal sebaceous glands.  Not present in preterm infants, and decreases in quantity after term.

·                     Traumatic cyanosis of the face Due to many small petechial haemorrhages in the skin after congestion of the head with the cord around the neck.

·                     Superficial skin peeling Common during the first week.  It is especially marked in post-term or wasted babies.

·                     Hair Colour at birth is poor guide to future shade.  Lanugo is fine facial and body hair which is a feature of preterm babies.

·                   Milia White pin-head size spots on the forehead, nose, upper lip, and cheeks.  These are tiny sebaceous retention cysts. Approximately 40% of newborn infants develop milia. Typically, the rash appears after 4-5 days in full-term newborns. Infants born prematurely are less commonly affected. The milia lesions range from 1-2 mm in size and are papular. These lesions are called Epstein pearls when present on the soft or hard palate.

Prognosis is excellent because milia is a benign self-limiting rash. Milial lesions disappear in a few days without leaving any scars.

·                     Miliaria – obstructed eccrine sweat ducts. Pinpoint vesicles on forehead scalp and skinfolds. Clear within 1 week.

·                     “Mucus burns” Red scald-like lesions around the mouth and cheeks due to regurgitated gastric juice (high hydrochloric acid content).

·                     “Mongolian spot“  Flat blue-black areas over sacrum or buttocks, and occasionally on back, shoulders, hands and feet.  Disappear by 4 years.

·                     Vascular naevi

o         Salmon patches:  superficial capillary haemangiomata may occur over the upper eyelids and on the nape of the neck (stork-bite).  They usually fade by 1 year.

o         Strawberry naevus: a raised capillary haemangioma with a surface resembling a strawberry.  At birth, the strawberry-to-be may show as a white (depigmented) patch of skin.  Growth is rapid and it may easily reach 4 cm in diameter.  It usually starts to subside by 1 year and most have disappeared by 7 years of age.  Surgical removal is rarely necessary.

o         Port wine mark (naevus flammeus):  may cover an extensive area.  It persists for life.  If situated over the ophthalmic division of the trigeminal nerve it may be associated with a meningeal haemangioma (Sturge-Weber syndrome).  Large marks may require laser treatment later.

·                   Erythema toxicum neonatorum Very common.  Red blotchy rash, associated with central pin-head papules (which may look like pustules but contain eosinophils) on the trunk, extremities, and the face. It occurrs between the second and eighth days.  Seldom seen in preterm infants. Individual lesions are transitory, often disappearing within hours and then appearing elsewhere on the body. They then tend to spread centripetally.

The etiology of ETN remains uncertain. ETN is a benign, asymptomatic, self-limited condition that requires no treatment. The lesions typically resolve within 2 weeks, and no cutaneous or systemic sequelae generally are observed.

 

 

·                     Fat necrosis  Localized areas of induration on back, thighs, or face (after forceps delivery).  It has a dark red appearance and may fluctuate.  Resolves spontaneously but needs to be differentiated from skin abscesses.

·                      Sclerema  Very firm rubbery feel to the skin.  Associated with severe infection, hypothermia or severe asphyxia.

·                      Wasting Dry, loose skin hangs in folds due to loss of muscle and subcutaneous fat resulting from recent intrauterine starvation.

Breasts  Breast enlargement is common in both male and female babies, usually lasting a week or two (but may persist for months).  It is due to the effect of oestrogen and progesterone.  No treatment is necessary.  Handling must be avoided as this may cause true mastitis.

Gastrointestinal tract

·                     Vomiting Babies normally swallow a variable quantity of air when feeding and commonly bring up a small amount of milk when winded.  Occasional large vomits without cause may occur.  Persistent vomiting however, should be assessed carefully and investigated especially if bile is present.

·                      Serious causes

o         alimentary tract obstruction due to atresia, meconium ileus, volvulus, strangulated hernia, inspissated milk, Hirschsprung’s disease and necrotising enterocolitis

o         marked gastro-oesophageal reflux

o         infection (including urinary tract)

o         cerebral pathology (including intracranial bleed or meningitis)

o         metabolic disorders

·                     Faeces

o         Meconium is passed within 48 hours of birth in the majority of babies.  (When passed in utero it usually indicates fetal distress).  Obstruction may rarely be caused by a firm meconium plug, and may be relieved by gently inserting a small glycerine suppository into the anus.

o         Stools replace meconium on day 3 or 4.

o         Breast milk stools are usually bright yellow (vary from orange to green), may vary from watery to pasty, and may contain mucus or milk curds.  Two to five stools are usually passed each day, but the variation ranges from one stool a week to 12 a day.

o         Cow’s milk (formula) stools are pale yellow, firmer and less frequent (up to 5 a day)

o         “Starvation stools” which occur in under-fed infants are characteristically small and dark green

o         Blood in stools is commonly due to swallowed maternal blood (distinguished from fetal blood by Apt test)

Renal function

·                     newborn infants should pass urine within the first 24 hours

·                     boys should pass urine with a good stream (dribbling suggests posterior urethral valves)

·                     in the first few weeks the infant empties his bladder up to 20 times a day

·                     urates may colour the urine heavily leaving a brick-red stain on the nappy (sometimes mistaken for blood)

·                     the newborn kidney is less able to excrete a solute load and has a reduced concentrating capacity in comparison with the older child

·                     Urine collection:  most easily done using a collecting bag, but contamination is a risk.  Uncontaminated urine may be obtained by suprapubic bladder puncture.

Genitalia

·                     term male infants usually have testes in the scrotum at birth.  The majority of incompletely descended testes come down within the first month

·                     preterm babies tend to have incompletely descended testes and a less well-developed scrotum

·                     fluid hernia (soft swelling of scrotum which transilluminates easily) is common.  Most disappear spontaneously within the first year

·                     foreskin is normally adherent to the glans penis and cannot be pulled back without trauma:  90% become fully retractable by the age of 3 years.  Pulling back the foreskin in infancy is therefore not advisable and routine circumcision is medically unnecessary

·                     a mucoid vaginal discharge is present iearly all mature female infants at birth

·                     vaginal bleeding occasionally occurs at the end of the first week (a hormone withdrawal effect of no pathological significance)

 

HYPOGLYCAEMIA

A newborn baby depends largely on glucose for his energy requirements. Glycogen is laid down in the liver with advancing gestation and provides the main source of glucose. Subcutaneous fat stores are also important. Milk feeds supply most energy after birth.

Normal Values: Fetal blood glucose is usually 2/3 of the maternal value. Blood glucose usually 2.5 mmol/l (45 mg %) to 5.0 mmol/l (90 mg %) during the first week of life

Definition:

·                     Blood glucose below 2.5 mmol/l (45 mg %)

·                     Reagent strips are used to screen for hypoglycamia.  The correct use of a reflectance meter has greatly increased the accuracy of readings but levels below 1.4 mmol/l should if possible be confirmed with a laboratory measurement.

·                     Infant is at risk of severe hypoglycaemia ( less than 1.4 mmol/l) if mild hypoglycaemia (1.4 to 2.5 mmol/l) is present.

Common Causes:

·                     Decreased glycogen stores (preterm baby; underweight for gestational age or wasted baby; late feeding)

·                     Increased demand for glucose (respiratory distress; hypothermia; infection)

·                     Increased insulin (infant of diabetic mother; Rh disease)

·                     Liver damage (hypoxia; infection)

Rare Cause: Pancreatic cell hyperplasia.

Clinical Presentation:

·                     Asymptomatic:

o         picked up when screening “at risk” babies

o         common when infants have mild hypoglycaemia but even infants with severe hypoglycaemia may be asymptomatic

·                     Symptomatic:

o         CNS effects:  poor sucking, lethargy, jitteriness, apnoea and cyanosis, convulsions

o         cardiac effects:  heart failure and respiratory distress

Note:  Persistent hypoglycaemia with symptoms results in severe brain damage in more than 30% of cases.

Treatment:

·                     Prevention:

o         Normal infants should be put to the breast immediately after delivery

o         Identify infants at risk of hypoglycaemia

o         It is particularly important that these infants be started on breast or full strength milk feeds soon after birth

o         Tube feed if necessary

o         Start intravenous fluids (Neonatalyte) if milk feeds are contraindicated

o         Blood glucose levels must be monitored every 1-3 hours for the first 24-48 hours

o         Avoid hypothermia

·                     Treatment of mild hypoglycaemia:

o         Give a milk feed

o         Keep the infant warm

o         Repeat the blood glucose measurement after 30 minutes

o         If mild hypoglycaemia persists repeat the feed with milk sweetened with sugar and again measure blood glucose after 30 minutes

o         If the reading is still below normal treat as for severe hypoglycaemia

·                     Treatment of severe or symptomatic hypoglycaemia:

o         Start intravenous infusion of 10% dextrose (Neonatalyte) 60 ml/kg/24 hours.  Insert umbilical vein catheter if unable to establish a peripheral line.

o         Measure blood glucose after 5 minutes.  If hypoglycaemia persists increase the intravenous dextrose to 15% (add 10 ml 50% glucose to 100 ml of Neonatalyte).  In addition 2.5 ml of 50% glucose can be given very slowly into the bulb of the infusion set.  Never give undiluted 50% glucose intravenously or orally as it is very hypertonic.

o         Hydrocortisone 5 mg intravenously if glucose therapy alone is not sufficient

o         Monitor blood glucose carefully with reagent strips

o         Start milk feeds, sweeten with sugar if needed, as soon as possible

In an emergency, if it is not possible to give intravenous glucose, small sweetened milk feeds can be given.  Do not give oral glucose feeds.

Conjugated Hyperbilirubinaemia This condition results from the failure of clearance from the body of the bilirubin, which has been already combined with glucuronic acid to form the soluble glucuronide. This generally implies an obstruction of large or small branches of the biliary tree. The problem is not so much the conjugated bilirubin, which is non-toxic, but the pathological underlying cause.

It is not normally necessary to treat the jaundice as the conjugated form is not toxic, but also because phototherapy given to such babies causes the “bronze baby” syndrome.

Treatment should focus on the underlying condition, once it is identified.

 

TEMPERATURE CONTROL

In the newborn, the temperature regulating mechanism is not as efficient as that of an older child and there is a much greater risk of excessive cooling or overheating.  At a normal skin temperature of 36-36.5°C (or an axillary temperature of 36.5-37°C) the newborn infant’s metabolic rate, as reflected by oxygen consumption, is reduced to a minimum.  This enables optimum use to be made of energy for purposes of growth.  Oral or rectal temperatures, useful in detecting fever, are rarely used iewborn infants.

The environmental temperature, which is needed to maintain this state, is dependent on the weight and post-natal age of the baby, and is influenced by humidity, air currents and clothing.  Thus, to provide a “neutral thermal environment”, the initial incubator temperature for the infant nursed naked in an incubator should be:

·                   32°C (range 31° – 34°C)  –  for a 3 kg infant

·                   34°C (range 33° – 35°C)  –  for a 2 kg infant

·                   35°C (range 34° – 36°C)  –  for a 1 kg infant

For the term infant, dressed and nursed in a bassinette, an environmental temperature of 20°C (range 18° – 22°C) should be adequate.

HYPOTHERMIA
This is defined as a temperature below 35°C.

·                     Predisposing factors:

o         Exposure

o         Low birth weight

o         Home delivery

·                     Heat is lost by:

o         conduction (if the infant is laid on a cold surface or wrapped in cold blankets)

o         convection (to surrounding air especially if in a draught or if cold oxygen administered)

o         evaporation (if baby is not dried promptly or if humidity is low)

o         radiation (especially if an “open” incubator is used, when heat is lost to cold windows and walls)

The low birth weight infant (preterm or underweight for gestational age) is particularly prone to hypothermia for the following reasons:

o                     larger surface area to body mass ratio

o                     less subcutaneous tissue with less insulation

o                     inadequate brown fat for non-shivering thermogenesis

o                     prone to hypoxia, hypoglycaemia and sepsis, all of which predispose to hypothermia

·                     Hypothermia in the low birth weight infant may result in:

o                     Hypoglycaemia

o                     Respiratory distress

o                     Increased 02 consumption

o                     Hypoxia and resultant metabolic acidosis

o                     Increased caloric requirement

o                     Poor weight gain

o                     Bleeding due to DIC.

o                     Neonatal cold injury

o                     Neonatal death

Management:

·                     Recognition:

o         Use “low reading” mercury thermometer or telethermometer

·                     Prevention:

o         Dry the infant immediately after birth then wrap in a second warm dry towel and give to mother or place in a warm cot or incubator.  Dry the head well.

o         If resuscitation is required this should be done on a suitably warmed surface with an overhead radiant heater.

o         Small babies, i.e. below 1800g, should be nursed in an incubator and abdominal skin temperature kept at 36.5°C. by adjusting the incubator temperature or using a servocontrolled incubator.

o         A perspex heat shield may be used to lessen radiant heat loss.

o         Use woollen caps in all low birth weight infants even if nursed in a closed incubator.  Dress infants when possible.

o         Use curtains in the newborursery.

Treatment of hypothermia:

1.                 Increase incubator temperature further or add overhead radiant heat source.

2.                 Increase room temperature if cold.

3.                 Use perspex heat shield and put on a warm woollen cap to minimize radiant heat loss from the scalp.

4.                 Monitor and treat hypoglycemia if present.

5.                 Give extra calories and oxygen while warming the infant.

6.                 Look for and treat any predisposing cause.

NEONATAL COLD INJURY

This refers to the unusual event of severe hypothermia.  Risk factors include birth during winter, home delivery and low birth weight.

Clinical features include apathy and poor feeding.  The cry is feeble and the infant is lethargic with depressed reflexes, bradycardia and oliguria.  The skin feels cold to the touch and is usually below 32°C  (May drop as low as 27°C).

The infant looks deceptively healthy with a ruddy face and extremities.
Oedema of the lower limbs may progress to sclerema (a woody feeling).

The mortality is high (25-35%) due mainly to:

·                      Hypoglycaemia (risk during re-warming)

·                      Hypoxaemia

·                      Pulmonary haemorrhage

Treatment:

·                     Rapid re-warming in an incubator, preferably using a servo- controlled overhead radiant heater

·                     Intravenous 10% dextrose water to prevent hypoglycaemia

·                     Antibiotics in view of high risk of infection

·                     Headbox 02 (e.g. 35% 02) during re-warming

FEVER

·                     Pyrexia is often due to overheating:

o         incubator or room temperature too high

o         lying in direct sunlight, or phototherapy

o         over-dressing the infant

Once these errors have been corrected, the temperature should return to normal within 1 hour.

If none of the above factors are operative or if the infant remains febrile or looks unwell the following should be considered and excluded:

·                     Infection

·                     Dehydration fever:

o          rarely seen to-day

o          usually a term infant who has fed poorly and lost more than 10% of his birth weight

o          temperature returns to normal within hours following ingestion of extra water between feeds

·                     Brain damage with hypothalamic injury

Discharge of healthy mothers and term babies before 48 h after birth (often within 24 h of birth) is a reality in many areas. Common components of most successful programs include the following:

·                     a normal vaginal birth with the baby having a normal adaptation to extrauterine life, and neither the mother nor the baby have ongoing problems requiring hospitalization;

·                     adequate preparation of the family for early discharge and access to community services after delivery, which may include home visits by health care personnel with maternal/infant experience and additional home care assistance as required;

·                     facilitation of maternal/infant contact in hospital, with decisions regarding early discharge individualized for both the baby and the mother.

 

2.  Fetal hypoxia and birth asphyxia

 

Background: In spite of major advances in monitoring technology and knowledge of fetal and neonatal pathologies, perinatal asphyxia (PA) remains a serious condition, causing significant mortality and long-term morbidity.

This is a syndrome characterized by clinical and laboratory evidence of acute brain injury due to asphyxia (ie, hypoxia, acidosis).

Frequency: Severe (stage 3-4) PA is rare; 2-4 cases per 1000 births are reported. Incidence in most technologically advanced nations of the world is the same as that in the United States.However, in developing nations the incidence of PA is likely to be higher. Accurate statistics are not available.

Mortality/Morbidity: In severe PA, the mortality rate is as high as 50%. Half of the deaths occur in the first month of life. Some infants with severe neurologic disabilities die in infancy from aspiration pneumonia and other infections.

Chronic antenatal fetal hypoxia

Causes:

Diseases of future mother:

·                   Anemia, leukemia

·                   Pulmonary and cardiovascular diseases

·                   Smoking, drug abuse

·                   Influence of toxins and chemical substances, some medicine

·                   Hemorrhages

Uterine-placental hemocirculation disturbances

·                   Pathology of placenta and its’ presentation

·                   Damage of placenta by infection

·                   Cord abnormalities

Diseases of the fetus

·                   Isoimmune incompatibility of mother and fetus

·                   TORCH-infections

·                   Fetal abnormalities

Pathogenesis: Lack of oxygen → Compensatory mechanisms activation → Anaerobe glycolysis → Catecholamine output → Circulation centralization → Methabolic acidosis → Concentration of the blood → Microthrombosis of the microcirculatory channel → Damage of all organs and systems with predominant damage of the brain → Decompensation → Suprarenal insufficiency Arterial hypotension → Shock.

Diagnostic criterions of fetal hypoxia

Antenatal            

·                   biophysical changes: changes of the cardiac rhythm, dullness of the cardiac tones, increased or decreased fetal movement,

·                   depending of the cardiac rate on the fetal movements, breathing movements, tonus, volume of the amniotic fluid

 Intranatal

·                   meconium in the amniotic fluid

·                   changes of the cardiac rhythm and breathing

·                   muscular hypotonia, hyporephlexia

·                   pallor or cyanosis of the skin

·                   changes of the blood gases

Birth asphyxia is a clinical neurological correlate of perinatal oxygen deprivation.

Asphyxia neonatorum is defined as a failure to establish spontaneous, regular respiration within a minute of birth.  Asphyxia neonatorum, with the associated clinical signs of cyanosis, bradycardia, hypotonia and a poor response to stimulation can be objectively assessed by the Apgar score.  All infants with a low 1 minute Apgar score, e.g. 6 or less, need some assistance.

Asphyxia neonatorum is a neonatal emergency as it may lead to hypoxia and possible brain damage or death if not correctly managed.  There are many causes of asphyxia neonatorum including prenatal hypoxia, maternal anaesthesia or sedation and preterm or difficult delivery.  Not all infants with asphyxia neonatorum have suffered prenatal hypoxia while prenatal hypoxia does not necessarily result in a low Apgar score.  It is therefore not surprising that the association between a low Apgar score and abnormal neurological development is tenuous.

The best marker of hypoxia in the hours before delivery is the presence of a metabolic acidosis at birth.  A base deficit greater than 10 in the blood of the umbilical artery suggests significant fetal hypoxia.  If possible the acid-base status of umbilical arterial blood should be determined in all cases of fetal stress or asphyxia neonatorum.

Anticipation is the key to good care, i.e. it is important to identify fetuses which are likely to be at risk of asphyxia, to monitor such high risk pregnancies during labour, to intervene appropriately, and to be adequately prepared for resuscitation.  The goal is to present each mother with a healthy newborn infant who has maximal potential for growth and development.

High risk pregnancies

Maternal status:
    Teenage (< 16)
    Elderly (> 40)
    Low socioeconomic status

Maternal illness:
    Diabetes
    Hypertension
    Rh sensitization
    Severe anaemia

Previous pregnancies:
    Previous abortions
    Previous stillbirths
    Previous early neonatal deaths
    Previous preterm infants

Present pregnancy:
    No antenatal care
    Hypertension
    Multiple pregnancy
    Polyhydramnios
    Abnormal presentation or position
    Certain drugs – alcohol, smoking
    Preterm labour
    Severe fetal growth retardation

High risk pregnancies should be delivered in hospitals where appropriate facilities are available.

Pathogenesis
Ischaemia and decreased oxygen delivery to the fetus/baby during the prepartum, intrapartum or immediate postpartum period, with hypoxic-ischaemic damage to the central nervous system and, in varying degrees, to the other body systems.

Apgar score
The 1 minute score indicates the need for resuscitation, while the 5 minute score gives an indication of the success of the resuscitation attempts.

Diagnostic criteria moderate – 4-6 balls on the 1^st minute with the improvement on the 5^th minute; severe – 0-3 balls on the 1^st minute, with the improvement on the 5^th minute; 5-6 balls on the 1^st and 5^th minute without improvement                                                                

Complications:

·                     Cardiovascular: Heart rate and rhythm disturbances, cardiac failure, hypotension.

·                     Pulmonary: Respiratory distress/respiratory failure, pulmonary hypertension, pulmonary haemorrhage.

·                     Renal: Renal failure, urinary retention.

·                     Gastrointestinal tract: Ileus, necrotising enterocolitis.

·                     Central nervous system: Increased intracranial pressure, cerebral oedema, encephalopathy, seizures, inappropriate antidiuretic hormone (ADH) secretion, hypotonia, hypertonia, apnoea.

·                     Metabolic: Hypoglycaemia, hypocalcaemia, hypomagnesaemia, metabolic acidosis.

·                     Body temperature: Hypothermia, hyperthermia.

·                     Other: Disseminated intravascular coagulation.

Heart and Lungs: Heart failure due to hypoxic ischaemic damage. Dilated cardiomyopathy, with increased tricuspid incompetence and poor contractility.
Beware of fluid overload during resuscitation.

Surfactant synthesis inhibited if pH < 7.25, predisposing to the development of neonatal respiratory distress due to surfactant deficiency.

Initial fall in pulmonary blood flow followed by a reactive hyperaemia. This may result in protein-rich fluid leak into the interstitium and alveoli causing a neonatal ‘ARDS’.

Massive pulmonary haemorrhage, usually secondary to left ventricular failure

Hepatorenal – Coagulopathy

·                     Oliguria due to acute tubular necrosis common.

o                     proteinuria, haematuria, myoglobinuria.

·                     Hepatic infarction possible adding to thromboplastin release and reduced synthesis of clotting factors.

·                     Coagulation abnormalities common.

o                     Usually secondary to disseminated intravascular coagulopathy.

o                     Not reversed by vitamin K.

§                                              Rx FFP

§                                              Cryoprecipitate if fibrinogen low

Gut and Biochemistry In the presence of hypoxia gut blood flow is reduced and redirected to essential organs.

 This may manifest in the early passage of meconium, and is more easily triggered nearer term.

If the asphyxia is severe enough, gasping may occur in utero leading to aspiration of meconium before birth.

Impaired gut bloodflow predisposes to poor tolerance of feeds necessitating a delay in starting milk.

Biochemical Markers indicative of asphyxia:

·                     Cord pH <7.0

·                     Elevated serum and particularly CSF lactate, especially if sustained.

·                     Brain ratios of organic:inorganic phosphate on MR spectroscopy.

CNS Hypoxic ischaemic encephalopathy (HIE) is the single most important cause of neonatal seizures with an incidence of 1-2 per 1000 live births.

Major manifestation of moderate or severe intra-partum asphyxia, and associated with long term sequelae in 20 – 40%.

Onset – usually within first day.
50% within 12 hours.
Often prolonged and difficult to control.

Motor abnormalities:

·                     Truncal hypotonia which reduces spontaneous movement.

·                     Focal weakness may relate to specific areas of injury.

·                     Bulbar / pseudobulbar palsy which will affect the child’s ability to swallow and feed.

Mechanisms of Brain Injury – Term infant

Global cerebral ischaemia usually underpins the cascade of events resulting in hypoxic-ischaemic brain injury.

The term infant is much more sensitive to the effects of such an insult.

Neuronal damage occurs in two major phases:

1.                 Primary cell loss with immediate hypoxic cellular damage and cell membrane dysfunction leading to neuronal death.

2.                 ‘Secondary energy failure’ describes the sequence resulting in further loss of neurons which starts around 6 hours after the insult and involves mitochondrial failure, the depletion of ATP from the neurons and the initiation of programmed cell death or apoptosis.

The degree of this secondary energy failure is a major determinant in survivors of neurodevelopmental outcome, and the window between insult and initiation of the process provides the stimulus for research into ways of limiting the neuronal damage.

Clinical manifestations and course vary depending on perinatal asphyxia severity.

Mild PA

·                   Muscle tone may be increased slightly and deep tendon reflexes may be brisk during the first few days.

·                   Transient behavioral abnormalities, such as poor feeding, irritability, or excessive crying or sleepiness, may be observed.

·                   By 3-4 days of life, the CNS examination findings become normal.

Moderately severe PA

·                   The infant is lethargic, with significant hypotonia and diminished deep tendon reflexes.

·                   The grasping, Moro, and sucking reflexes may be sluggish or absent.

·                   The infant may experience occasional periods of apnea.

·                   Seizures may occur within the first 24 hours of life.

·                   Full recovery within 1-2 weeks is possible and is associated with a better long-term outcome.

·                   An initial period of well-being may be followed by sudden deterioration, suggesting reperfusion injury; during this period, seizure intensity might increase.

Severe HIE

·                   Stupor or coma is typical. The infant may not respond to any physical stimulus.

·                   Breathing may be irregular, and the infant often requires ventilatory support.

·                   Generalized hypotonia and depressed deep tendon reflexes are common.

·                   Neonatal reflexes (eg, sucking, swallowing, grasping, Moro) are absent.

·                   Disturbances of ocular motion, such as a skewed deviation of the eyes, nystagmus, bobbing, and loss of “doll’s eye” (ie, conjugate) movements may be revealed by cranial nerve examination.

·                   Pupils may be dilated, fixed, or poorly reactive to light.

·                   Seizures occur early and often and may be initially resistant to conventional treatments. The seizures are usually generalized, and their frequency may increase during the 2-3 days after onset, correlating with the phase of reperfusion injury. As the injury progresses, seizures subside and the EEG becomes isoelectric or shows a burst suppression pattern. At that time, wakefulness may deteriorate further, and the fontanelle may bulge, suggesting increasing cerebral edema.

·                   Irregularities of heart rate and BP are common during the period of reperfusion injury, as is death from cardiorespiratory failure.

 

Infants who survive severe PA

·                   The level of alertness improves by days 4-5 of life.

·                   Hypotonia and feeding difficulties persist, requiring tube feeding for weeks to months.

Involvement of multiple organs besides the brain is a hallmark of HIE.

·                   Severely depressed respiratory and cardiac functions and signs of brainstem compression suggest a life-threatening rupture of the vein of Galen (ie, great cerebral vein) with a hematoma in the posterior cranial fossa.

·                   Reduced myocardial contractility, severe hypotension, passive cardiac dilatation, and tricuspid regurgitation are noted frequently in severe HIE.

·                   Patients may have severe pulmonary hypertension requiring assisted ventilation.

·                   Renal failure presents as oliguria and, during recovery, as high-output tubular failure, leading to significant water and electrolyte imbalances.

·                   Intestinal injuries may not be apparent in the first few days of life. Poor peristalsis and delayed gastric emptying are common; necrotizing enterocolitis occurs rarely.

HIE – Grading and prognosis The staging system proposed by Sarnat and Sarnat in 1976 is often useful.

Stages of hypoxic-ischaemic encelphalopathy (HIE)
Stage	Stage 1 (mild)	Stage 2 (moderate)	Stage 3 (severe)
Level of consciousness	Hyperalert; irritable	Lethargic or obtunded	Stuporous, comatose.
Neuromuscular control:	Uninhibited, over-reactive	Diminished spontaneous movement	Diminished or absent spontaneous movement
Muscle tone	Normal	Mild hypotonia	Flaccid
Posture	Mild distal flexion	Strong distal flexion	Intermittent decerebration
Stretch reflexes	Over-active	Over-active, disinhibited	Decreased or absent
Segmental myoclonus	Present or absent	Present	Absent
Complex reflexes:	Normal	Suppressed	Absent
Suck	Weak	Weak or absent	Absent
Moro	Strong, low threshold	Weak, incomplete high threshold	Absent
Oculovestibular	Normal	Over-active	Weak or absent
Tonic neck	Slight	Strong	Absent
Autonomic function:	Generalised sympathetic	Generalised sympathetic	Both systems depressed
Pupils	Mydriasis	Miosis	Mid-position, often unequal; poor light reflex
Respirations	Spontaneous	Spontaneous; occasional apnoea	Periodic; apnoea
Heart rate	Tachycardia	Bradycardia	Variable
Bronchial and salivary secretions	Sparse	Profuse	Variable
Gastrointestinal motility	Normal or decreased	Increased diarrhoea	Variable
Seizures	None	Common focal or multifocal (6–24 hours of age)	Uncommon (excluding decerebration)
Electro-encephalographic findings	Normal (awake)	Early: generalised low-voltage, slowing (continuous delta and theta) Later: periodic pattern (awake); seizures focal or multifocal; 1.0 to 1.5 Hz spike and wave	Early: periodic pattern with isopotential phases Later: totally isopotential
Duration of symptoms	less than 24 hours	2 to 14 days	Hours to weeks
Outcome	About 100% normal	80% normal; abnormal if symptoms more than 5 to 7 days	About 50% die; remainder with severe sequelae

 

Steps to resuscitate a newborn infant (ABC resusitation)

 

If the infant does not breathe well at delivery, stimulate by flicking the feet.  This usually results in a good cry.  Drying the infant may also stimulate the onset of respiration.

If stimulation fails to initiate regular respiration, gently suction the oropharynx with a soft catheter.  When the infant is covered with thick meconium it is important to clear the airway before respiration is initiated i.e. before delivery of the shoulders.  A large end-hole catheter (F12) is preferred when clearing meconium.

When stimulation and a clear airway do not result in adequate respiration, give 100% oxygen via a face mask and again stimulate the infant.  A few gasps of oxygen are usually successful in establishing respiration.

If the infant is still not breathing, some form of artificial ventilation is required.  The simplest method is mask ventilation using a resuscitator (Laerdal, Ambu, Samson) with the mask applied tightly to the infant’s face.  Failing this, the infant should be intubated with a 2,0 or 2,5 mm endotracheal tube using a laryngoscope with a size “0” straight blade.  The resuscitator can then be connected to the endotracheal tube.  Forty breaths a minute is recommended.  The chest should move and air entry should be heard on both sides of the chest.

Endotracheal intubation is a simple procedure which should be learned by all staff dealing with infants at delivery.

The more severe the fetal hypoxia the longer it will take before the infant starts to breathe spontaneously.  Pulse rate, measured by palpating the base of the umbilical cord or auscultating the heart, should be above 100 per minute.

Naloxone (Narcan) 0,25 ml/kg (i.e. 0,1 mg/kg) can be given IV or IM or down the endotracheal tube if the mother has received pethidine or morphine within 4 hours of delivery.  Usually 0,75 ml is given to term infants and 0,5 ml to preterm infants.  Naloxone only reverses the respiratory depressing effects of opiate analgesics.  It should not be given routinely to all infants born to women who have received analgesia.  Neonatal Narcan is no longer used as the dose is too small.

If the infant does not breathe despite adequate ventilation, or if heart rate remains below 80 beats per minute, give external cardiac massage with two fingers depressing the lower sternum at approximately 100 times a minute while continuing with respiratory assistance. 

 Adrenaline 0,25 ml/kg of a 1:10 000 solution (i.e. 1 ml adrenaline 1:1000 diluted in 10 ml saline) in can also be placed down the endotracheal tube or be given  IV.

If the heart rate still remains slow,
Give 5 ml of 4% sodium bicarbonate slowly into the umbilical or a peripheral vein.  Never give any medication into the umbilical artery.  Use 5 ml 8% sodium bicarbonate mixed with 5 ml normal saline if 4% sodium bicarbonate is not available.

Check the blood glucose concentration.  If below 1.4 mmol/l (25 mg %) give 5 ml 25% dextrose water slowly intravenously.
If the infant appears exsanguinated (e.g. from a snapped cord) give 20 ml/kg of Haemaccel, stabilised human serum or blood.

Once the infant is resuscitated it should be transferred to the nursery for observation and further assessment.

Treatment guidelines

Management		Comments
Non-drug treatment	Resuscitation. Oxygen to keep Pao2 between 60 and 80 mmHg. Ventilatory support if Paco2 > 50 mmHg and/or Pao2 < 60 mmHg. Maintain blood glucose at 2.5–6 mmol/L. Maintain haematocrit at ³ 40%. (Packed red cells, IV, 10 mL/kg.) Maintain blood pressure at 70/45 in a term infant or 50/35 in a pre-term infant.	Admit to neonatal high care or neonatal intensive care facility. Neutral thermal environment. 1 kPa = 7.5 mmHg; 1 mmHg x 0.133 = 1 kPa
IV Fluids:	Restrict fluids to 50–60 mL/kg in first 24–48 hours. Frequent assessment of fluid balance (intake and output). Use 10% dextrose water or a potassium-free neonatal maintenance solution until the possibility of renal failure has been excluded. Maintain serum electrolytes, calcium, magnesium and acid–base status withiormal physiological range.
Nutrition:	No enteral feeds for at least the first 24 hours. Enteral milk feeds only after ileus has been excluded. Consider IV alimentation if enteral feeds are still not possible after 72 hours.
Monitor:	Neurological status, vital signs, acid–base status, blood gases, SaO2, blood pressure, fluid balance, temperature, blood glucose, electrolytes, minerals, osmolality, renal function.	Follow-up by medical practitioner or at clinic/hospital.
Drug treatment	Vitamin K1, IM, pre-term infants 0.5 mg; full term infants 1 mg.
Suspected infection:	Cefotaxime, IV, 50–100 mg/kg/24 hours in 2–3 divided doses for 10 days.	Give IV antibiotics (3rd generation cephalosporin) if infection is suspected.
Hypotension:	Fresh frozen plasma, IV, 20 mL/kg over 1 hour	Treat complications, e.g. hypotension, convulsions, renal failure, inappropriate ADH secretion, cardiac failure, etc.
	AND Dopamine, IV, 5–15 micrograms/kg/minute OR Dobutamine, IV, 5–15 micrograms/kg/minute until blood pressure is stabilised.

 

Convulsions:	Phenobarbital, IV loading dose 20 mg/kg, followed by maintenance of 5–10 mg/kg/24 hours as a single dose or in 2 divided doses.
	OR Phenytoin, IV loading dose 15 mg/kg, followed by maintenance of 5–10 mg/kg/24 hours as a single dose or 2 divided doses.	If response is unsatisfactory, consider use of other anticonvulsants, e.g. clonazepam.
Cardiac failure:	Fluid restriction, diuretics and digoxin. Furosemide, oral/nasogastric tube or IV, 1 mg/kg/24 hours as a single daily dose. Digoxin, IV, 0.01 mg/kg/dose 8 hourly for 3 doses, followed by 0.01 mg/kg/24 hours in 2 divided doses.
Hypocalcaemia:	Serum total calcium < 1,7 mmol/L or ionised calcium < 0.7 mmol/L: Calcium gluconate 10%, slow IV, 0.2–0.5 mL/kg over 15 minutes, under ECG control.	Calcium gluconate 10% contains 0.225 mmol calcium/mL.
Hypomagnesaemia:	Serum magnesium < 0.7 mmol/L: Magnesium sulphate 50%, IV, 0.2 mL/kg as a single dose.
Hypoglycaemia:	Blood glucose < 2,5 mmol/L: Dextrose, IV as bolus, 250–500 mg/kg.	Dilute 50% dextrose solution before use. 250–500 mg/kg = 0.5–1 mL/kg of 50% dextrose.
Inappropriate ADH:	Fluid restriction.
Cerebral oedema / raised intracranial pressure:	Raise head of cot by 10–15 cm. Furosemide, IV, 1 mg/kg as single dose. (Do not repeat.) Moderate hyperventilation to lower Paco2 to 28–35 mmHg. Mannitol 25% solution, IV, 2 mL/kg over 30 minutes. (Do not repeat.) Moderate fluid restriction (50–60 mL/kg/24 hours) for the first 24–48 hours.	Control cerebral oedema and increased intracranial pressure. Steroids are considered unhelpful. 1 kPa = 7.5 mmHg; 1 mmHg x 0.133 = 1 kPa

Ethical Issues

Outlook at resuscitation is very poor if there is no cardiac output at 15 minutes of life or if the heart rate responds but there is no regular respiration at 30 minutes.

Treatment following perinatal asphyxia is initially supportive, trying to maintain homeostasis while making an assessment of the severity of the hypoxic-ischaemic insult.
It is difficult to predict the severity of long term sequelae if there is an initial response to resuscitation. The infant’s apnoea may have resolved, and he/she may be breathing spontaneously by the time it is apparent there will be major neurodevelopmental delay resulting from the asphyxial insult.

There is still no good crystal ball, and because the asphyxial insult is global, the long term effect may manifest across all aspects of development.

Prevention:

The era of neuroprotection may be near. Most of the treatments discussed here are experimental. With the exception of hypothermia, which is still being examined in clinical trials, none of the therapies cited below has been consistently shown to have efficacy in human infants.

o                     Allopurinol: Slight improvements in survival and CBF were noted in a small group of infants tested with this free-radical scavenger in one clinical trial.

o                     High-dose phenobarbital: In another study, 40 mg/kg phenobarbital was given over 1 hour to infants with severe HIE. Treated infants had fewer seizures (9 of 15) than untreated control infants (14 of 16). Treated infants also had fewer neurological deficits at age 3 years (4 of 15) than untreated infants (13 of 16). This is the only study showing a benefit of this magnitude in using high-dose phenobarbital for severe HIE. As of this writing, this treatment is not considered the standard of care.

o         EAA antagonists: MK-801, an EAA antagonist, has shown promising results in experimental animals and in a limited number of adult trials. It has not been tested iewborn infants. This drug has serious cardiovascular adverse effects.

o         Hypothermia: Currently being intensely tested as a neuroprotective therapy, hypothermia’s mechanism of protection is not completely understood. Explanations include (1) reduced metabolic rate and energy depletion; (2) decreased excitatory transmitter release; (3) reduced alterations in ion flux; and (4) reduced vascular permeability, edema, and disruptions of blood-brain barrier functions. The current state-of-the-art on hypothermia is summarized by the following:

·                     Brain cooling to about 3-4°C below the baseline temperature (ie, to 33-34°C) may be neuroprotective. The optimal level of hypothermia for maximal neuroprotection is not known. Extreme hypothermia may cause significant systemic side effects.

·                     Up to 48-72 hours of cooling may be needed to prevent secondary neuronal loss. The greater the severity of the initial injury, the longer the duration of hypothermia needed for optimal neuroprotection.

·                     Cooling must be begun early, within 1 hour of injury, if possible; however, favorable outcome may be possible if cooling is begun up to 6 hours after injury.

·                     A special device that selectively cools the head is now being tested in clinical studies; it is not available in the market. Some investigators believe that total body cooling (as done for open-heart surgery) may be superior to selective head cooling. The relative merits and limitations of different methods of brain cooling have not been studied.

·                     Hypothermia may cause significant side effects, including coagulation defects, leukocyte malfunctions, pulmonary hypertension, and worsening of metabolic acidosis. Until more is learned, hypothermia remains an experimental modality.

 

Birth traumas.

 

INTRODUCTION Injuries to the infant resulting from mechanical forces (ie, compression, traction) during the process of birth are categorized as birth trauma. Factors responsible for mechanical injury may coexist with hypoxic-ischemic insult. One may predispose the infant to the other. Lesions that are predominantly hypoxic in origin are not discussed in this article. Significant birth injury accounts for fewer than 2% of neonatal deaths and stillbirths in this country. It still occurs occasionally and unavoidably with an average of 6-8 injuries per 1000 live births. In general, larger infants are more susceptible to birth trauma. Higher rates are reported for infants over 4500 grams.

Most birth traumas are self-limiting and have a favorable outcome. Nearly half are potentially avoidable with recognition and anticipation of obstetric risk factors. Infant outcome is the product of multiple factors. Separating the effects of a hypoxic-ischemic insult from those of traumatic birth injury is difficult.

Risk factors include large-for-date infants, especially larger than 4500 grams; instrumental deliveries, especially forceps (midcavity) or vacuum; vaginal breech delivery; and abnormal or excessive traction during delivery.

Mortality/morbidity Birth injuries account for fewer than 2% of neonatal deaths. From 1970-1985, rates of infant mortality resulting from birth trauma fell from 64.2 to 7.5 deaths per 100,000 live births, a remarkable decline of 88%. This decrease reflects, in part, the technologic advancements for today’s obstetrician to recognize birth trauma risk factors by ultrasonography and fetal monitoring prior to attempting vaginal delivery. Use of potentially injurious instrumentation such as midforceps rotation and vacuum delivery has also declined. The accepted alternative is a cesarean delivery.

Causes The process of birth is a blend of compression, contractions, torques, and traction. When fetal size, presentation, or neurologic immaturity complicates this event, such intrapartum forces may lead to tissue damage, edema, hemorrhage, or fracture in the neonate. The use of obstetric instrumentation may further amplify the effects of such forces or may induce injury alone. Under certain conditions, delivery by cesarean delivery can be an acceptable alternative, but it does not guarantee an injury-free birth. Factors predisposing to injury include the following:

·                     Prima gravida

·                     Cephalopelvic disproportion, small maternal stature, maternal pelvic anomalies

·                     Prolonged or rapid labor

·                     Deep transverse arrest of descent of presenting part of the fetus

·                     Oligohydramnios

·                     Abnormal presentation (breech)

·                     Use of midcavity forceps or vacuum extraction

·                     Versions and extractions

·                     Very low birth weight infant or extreme prematurity

·                     Fetal macrosomia

·                     Large fetal head

·                     Fetal anomalies

INJURIES WITH FAVORABLE LONG-TERM PROGNOSIS

·                     Soft tissue

o                     Abrasions

o                     Erythema petechia

o                     Ecchymosis

o                     Lacerations

o                     Subcutaneous fat necrosis

·                     Skull

o                     Caput succedaneum

o                     Cephalhematoma

o                     Linear fractures

·                     Face

o                     Subconjunctival hemorrhage

o                     Retinal hemorrhage

·                     Musculoskeletal injuries

o                     Clavicular fractures

o                     Fractures of long bones

o                     Sternocleidomastoid injury

·                     Intra-abdominal injuries

o                     Liver hematoma

o                     Splenic hematoma

o                     Adrenal hemorrhage

o                     Renal hemorrhage

·                     Peripheral nerve

o                     Facial palsy

o                     Unilateral vocal cord paralysis

o                     Radial nerve palsy

o                     Lumbosacral plexus injury

SOFT TISSUE INJURY Soft tissue injury is associated with fetal monitoring, particularly with fetal scalp blood sampling for pH or fetal scalp electrode for fetal heart monitoring, which has a low incidence of hemorrhage, infection, or abscess at the site of sampling.

Cephalhematoma

 

 

 

 

 

 

 

 

Cephalhematoma is a subperiosteal collection of blood secondary to rupture of blood vessels between the skull and the periosteum; suture lines delineate its extent. Most commonly parietal, cephalhematoma may occasionally be observed over the occipital bone.

The extent of hemorrhage may be severe enough to cause anemia and hypotension. Resolving hematoma predisposes to hyperbilirubinemia. Rarely, cephalhematoma may be a focus of infection leading to meningitis or osteomyelitis. Linear skull fractures may underlie a cephalhematoma (5-20% of cephalhematomas). Resolution occurs over weeks, occasionally with residual calcification.

No laboratory studies usually are necessary. Skull radiography or CT scanning is used if neurologic symptoms are present. Usually, management consists of observation only. Transfusion and phototherapy are necessary if blood accumulation is significant. Aspiration is more likely to increase the risk of infection. The presence of a bleeding disorder should be considered. Skull radiography or CT scanning is also used if concomitant depressed skull fracture is a possibility.

 

Location of injury in soft tissue planes on the scalp and head.

 

Subgaleal hematoma

Subgaleal hematoma is bleeding in the potential space between the skull periosteum and the scalp galea aponeurosis. Ninety percent of cases result from vacuum applied to the head at delivery. Subgaleal hematoma has a high frequency of occurrence of associated head trauma (40%), such as intracranial hemorrhage or skull fracture. The occurrence of these features does not correlate significantly with the severity of subgaleal hemorrhage.

The diagnosis is generally a clinical one, with a fluctuant boggy mass developing over the scalp (especially over the occiput). The swelling develops gradually 12-72 hours after delivery, although it may be noted immediately after delivery in severe cases. The hematoma spreads across the whole calvarium. Its growth is insidious, and subgaleal hematoma may not be recognized for hours. Patients with subgaleal hematoma may present with hemorrhagic shock. The swelling may obscure the fontanelle and cross suture lines (distinguishing it from cephalhematoma). Watch for significant hyperbilirubinemia. The long-term prognosis generally is good.

Laboratory studies consist of a hematocrit evaluation. Management consists of vigilant observation over days to detect progression. Transfusion and phototherapy may be necessary. Investigation for coagulopathy may be indicated.

Caput succedaneum

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

 

 

 

 

 

 

 

 

 

 

 

Differential of cephalhematoma and caput succedaneum:

criterions	Cephalhematoma	Caput succedaneum
Situation on the head skin in this region fluctuation symptom peripheral roller dynamic    prolonged jaundice	Limited by one bone Without changes + + disappears in the month period +	Situated along few bones Cyanotic with petechiae –– –– disappears in 3-4 days   ––

 Abrasions and lacerations

Abrasions and lacerations sometimes may occur as scalpel cuts during cesarean delivery or during instrumental delivery (ie, vacuum, forceps). Infection remains a risk, but most heal uneventfully.

Management consists of careful cleaning, application of antibiotic ointment, and observation. Bring edges together using Steri-Strips. Lacerations occasionally require suturing.

Common Birthmarks and Minor Skin Conditions in the Newborn

There are a number of skin conditions that are considered normal in the newborn. There may be bruises or marks from forceps on the newborn’s face and scalp, or bruising of the feet following a breech delivery, all of which resolve within just a few days. Pink marks that are due to dilated capillaries under the skin may be seen on the forehead just above the nose, in the upper eyelids, or at the back of the neck (where it is called “stork-bite”). This type of birthmark fades as the infant grows but in some people remains as a faint mark that becomes brighter when the person becomes excited or upset. Some newborns have a few acne pimples, especially over the cheeks and forehead. These go away, and the only recommended action is to keep the skin clean and not to use creams or lotions.

Milia are tiny, pearly white cysts that are normally found over the nose and upper cheeks. Milia become smaller or disappear over a period of weeks. Similar white cysts are sometimes found on the gums or in the midline of the roof of the mouth (Epstein’s pearls) and are also of no consequence.

Mongolian spots are bluish gray, flat areas that usually occur over the lower back or buttocks. At first glance they appear to be bruises but are not. They are usually seen in black or Asiaewborns and are of no consequence.

A “strawberry hemangioma” is a common birthmark. It is a flat, slightly pink or red area anywhere on the skin. Over a period of weeks, it becomes darker red and also becomes raised up over the surface of the skin, appearing much as a strawberry. After several years, strawberry hemangiomas shrink and become fainter, so that by the time the child reaches school age, most are no longer visible. For this reason, surgery is not needed.

 

Subcutaneous fat necrosis

Subcutaneous fat necrosis is not usually detected at birth. Irregular, hard, nonpitting, subcutaneous plaques with overlying dusky red-purple discoloration on the extremities, face, trunk, or buttocks may be caused by pressure during delivery. No treatment is necessary. Subcutaneous fat necrosis sometimes calcifies.

 

Intracranial hemorrhages

Intracranial hemorrhages very often occur in premature newborns (25% – 40% of all newborns weighting less then 2000g). They are germinal matrix hemorrhages, are classified as grade I, II, and III.

 

 

Classification

Grade	Radiological Appearance – Site of Hemorrhage
I	Subependymal region and/or germinal matrix
II	Subependymal hemorrhage with minimal filling (10-40%) of lateral ventricles with no or little ventricular enlargement
III	Subependymal hemorrhage with significant filling of lateral ventricles (>50%) with significant ventricular enlargement
IV	Intraparenchymal hemorrhage

 

Grade I hemorrhages can be asymptomatic, often are diagnosed by ultrasonography.

In hard cases hemorrhage manifests by sudden catastrophic onset of seizures, anemia and cardiovascular instability.

Diagnostic criterions of intracranial hemorrhages

Epidural and subdural hemorrhages

·                   Vomiting

·                   Seizures

·                   Breathing and cardiac arrhythmia

·                   Hypothermia

·                   Hypotonia of muscles

·                   Hypertension-hydrocephalus syndrome, which increases

Subarachnoid hemorrhages

·                   Often apnea and secondary asphyxia

·                   Bradycardia

·                   Hypotonia of muscles, hyporephlexia

·                   Hyperesthesia

·                   Seizures

·                   Fixed glance

·                   Strained large fontanel 

Intracranial hemorrhages

·                   Coma

·                   Severe breathing and cardiac disturbances

·                   Tonic seizures, opistotonus

·                   Anisocoria, narrowing of ocular fissures, “swimming eye apples”

Hemorrhage into the brain

·                   Anxiety

·                   Mimic muscles seizures

·                   Absence of unconditional reflexes

The diagnosis of intracranial hemorrhages should be depend on: anamnestic data, clinical signs and symptoms, liquor investigation, neurosonography, ophthalmoscopy,

reoencephalography, computer tomography.

Imaging Studies Computer tomography is necessary for full evaluation of the cerebral parenchyma, the posterior fossa, and the subarachnoid, subdural, and epidural spaces.

o         Sonography is the diagnostic tool of choice for screening examination and follow-up of individuals with periventricular-intraventricular hemorrhage. Screening is best performed wheeonates are aged 3-7 days because most hemorrhages occur before that age. Late screening (ie, when individual is approximately aged 28 days) is useful to find the less common late hemorrhage.

o          Sonography is also the diagnostic tool of choice for the follow-up of individuals with PVH-IVH and posthemorrhagic hydrocephalus. Serial sonography is indicated weekly to follow for progression of hemorrhage and the development of posthemorrhagic hydrocephalus.

CT scan Prior to the availability of sonography, CT scanning was used for diagnosis and follow-up. CT scanning is no longer used for diagnosis and follow-up in view of the safety and cost effectiveness of sonography.

Although not as useful as sonography, frontal-occipital circumference can be used as an adjunct test in monitoring the progression of posthemorrhagic hydrocephalus.

Differentials Apnea of Prematurity, Hypermagnesemia, Hypoglycemia, Neonatal Sepsis, Periventricular Leukomalacia.

Criterions	Intracranial birth injury	meningitis
anamnestic data first signs appear   intoxication cerebral coma blood count   liquor	Abnormal delivery On 1-3 days of life Continue 10-12 days –– develops rapidly anemia   contains erythrocytes	Septic anamnesis After 3 days of life up to one month +++ develops slowly anemia, leukocytosis, left shift of leukocyte formula lymphocyte or neutrophil pleocytosis

 

 Treatment

·                   quiet

·                   head fixation, craniocerebral hypothermia

·                   feeding through nasogastral tube

·                   hemostatics (vicasolum 1% – 0,3 IM)

·                   dehydration therapy (lasix 1% – 0,3 IV)

·                   microcirculation improvement (rheopolyglucini10 ml/kg IV)

·                   Treatment of seizures.

·                   Treatment of secondary infections.                       

·                   Correction of fluid, electrolytes, and acid-base disturbances.

·                   Stabilizing and supporting the cardiovascular system.

·                   Treatment of renal, gastrointestinal disturbances.

·                   Symptomatic treatment  

·                   For patients with progressive ventriculomegaly and hydrocephalus, ventricular drains and subsequent ventriculoperitoneal shunting are often required.

Prognosis:

·                     Grade I and grade II hemorrhage: Neurodevelopmental prognosis is excellent (ie, perhaps slightly worse than infants of similar gestational ages without PVH-IVH).

·                     Grade III hemorrhage without white matter disease: Mortality is less than 10%. Of these patients, 30-40% have subsequent cognitive or motor disorders.

Grade IV (severe PVH-IVH) IVH with either periventricular hemorrhagic infarction and/or periventricular leukomalacia: Mortality approaches 80%. A 90% incidence of severe neurological sequelae including cognitive and motor disturbances exists

 

PERIPHERAL NERVE INJURY

What are Brachial Plexus Injuries?
The brachial plexus is a network of nerves that control the muscles of the shoulder, arm, elbow, wrist, hand and fingers. Injury to nerves of the brachial plexus can result in full to partial paralysis of one or both arms (bilateral brachial plexus injury).

Possible symptoms of a brachial plexus injury include: a limp or paralyzed arm; lack of muscle control in the arm or hand. Other terms commonly used to describe brachial plexus injuries include: Erb’s Palsy (upper trunk injury), Klumpke’s Palsy (lower trunk injury), Brachial Plexus Palsy, Erb-Duchenne Palsy, Horner’s Syndrome (when facial nerves are also affected), and “Burners” or “Stingers” (usually associated with sports-related brachial plexus injuries). Torticollis is another term sometimes used in conjunction with brachial plexus injuries.
What is the Brachial Plexus?
The brachial plexus is a network of nerves. It conducts signals from the spine to the arm and hand. These signals cause the arm and hand muscles to move. (Brachial means arm, and plexus refers to a network of nerves.)
What causes brachial plexus injuries?
Stretching, tearing, or other trauma can cause injury to the nerves of the brachial plexus. Brachial plexus injuries most often occur during the birthing process (Obstetrical Brachial Plexus Injury) as a result of excessive traction or force being applied to the infant’s head during delivery.

Approximately 2-3 or every 1000 newborns are affected by brachial plexus birth injuries. More children suffer from brachial plexus injuries sustained at birth than Down’s Syndrome or Muscular Dystrophy – yet information on this disability is not so readily obtained. Other frequent causes of brachial plexus injuries include: automobile, motorcycle or boating accidents; sports injuries; animal bites; and gunshot or puncture wounds.
What treatment options are available for brachial plexus injuries?
It is essential that treatment for a brachial plexus injury be obtained as soon as possible from qualified, experienced medical professionals who specialize in treating brachial plexus injuries.

Early treatment for brachial plexus injuries most likely will include occupational and/or physical therapy to help maximize use of the affected arm while preventing contactures (tightening of the muscles and joints).

While each brachial plexus injury is unique, some individuals may benefit form surgery. Highly specialized and experienced surgeons utilize a variety of operative approaches in attempting to maximize an individual’s function. Infants with brachial plexus birth injuries who show little or no improvement by the age of 4-6 month are often candidates for immediate surgery. Older children and adults may benefit from different surgical techniques as well.

It is important to note that even with ongoing therapy treatment and surgical intervention, complete recovery from a brachial plexus injury may not occur. Maximizing functional use of the injured arm in generally the overall goal of affected individuals, families and medical professionals.

 

Brachial plexus injury

Brachial plexus injury occurs most commonly in large babies, frequently with shoulder dystocia or breech delivery. Incidence for brachial plexus injury is 0.5-2.0 per 1000 live births. Most cases are Erb palsy; entire brachial plexus involvement occurs in 10% of cases.

 

Traumatic lesions associated with brachial plexus injury are fractured clavicle (10%), fractured humerus (10%), subluxation of cervical spine (5%), cervical cord injury (5-10%), and facial palsy (10-20%). Erb palsy (C5-C6) is most common and is associated with lack of shoulder motion. The involved extremity lies adducted, prone, and internally rotated. Moro, biceps, and radial reflexes are absent on the affected side. Grasp reflex is usually present. Five percent of patients have an accompanying (ipsilateral) phrenic nerve paresis.

Klumpke paralysis (C7-8, T1) is rare, resulting in weakness of the intrinsic muscles of the hand; grasp reflex is absent. If cervical sympathetic fibers of the first thoracic spinal nerve are involved, Horner syndrome is present.

No uniformly accepted guidelines for determining prognosis exist. Narakas developed a classification system (types I-V) based on the severity and extent of the lesion, providing clues to the prognosis in the first 2 months of life. According to the collaborative perinatal study (59 infants), 88% of cases resolved in the first 4 months, 92% by 12 months, and 93% by 48 months. In another study of 28 patients with upper plexus involvement and 38 with total plexus palsy, 92% recovered spontaneously.

Residual long-term deficits may include progressive bony deformities, muscle atrophy, joint contractures, possible impaired growth of the limb, weakness of the shoulder girdle, and/or Erb engram flexion of the elbow accompanied by adduction of shoulder.

Workup consists of radiographic studies of the shoulder and upper arm to rule out bony injury. The chest should be examined to rule out associated phrenic nerve injury. Electromyography (EMG) and nerve conduction studies occasionally are useful. Fast spin-echo MRI can be used to evaluate plexus injuries noninvasively in a relatively short time, minimizing the need for general anesthesia. MRI can define meningoceles and may distinguish between intact nerve roots and pseudomeningoceles (indicative of complete avulsion). Carefully performed, intrathecally enhanced CT myelography may show preganglionic disruption, pseudomeningoceles, and partial nerve root avulsion. CT myelography is more invasive and offers few advantages over MRI.

Management consists of prevention of contractures. Immobilize the limb gently across the abdomen for the first week and then start passive range of motion exercises at all joints of the limb. Use supportive wrist splints. Best results for surgical repair appear to be obtained in the first year of life. Several investigators recommend surgical exploration and grafting if no function is present in the upper roots at 3 months of age, although the recommendation for early explorations is far from universal. Complications of brachial plexus exploration include infection, poor outcome, and burns from the operating microscope. Patients with root avulsion do not do well. Palliative procedures involving tendon transfers have been of some use. Latissimus dorsi and teres major transfers to the rotator cuff have been advocated for improved shoulder function in Erb palsy. One permanent and 3 transitory axillary nerve palsies have been reported from the procedure.

Differential

Criterions	Brachial plexus injury	osteomyelitis
Anamnestic data Signs appear intoxication palpation   laboratory changes	Pathologic delivery From the first day of life –– painless, edema is absent   no changes	Septic anamnesis On 2-3 week of life ++ edema, tenderness of the arm anemia, leukocytosis, left shift of leukocyte formula

 

Erb’s Palsy (Brachial Plexus Birth Injury)

Erb’s palsy is a form of brachial plexus palsy.

Erb’s palsy leads to a weakness of a newborn baby’s arm. It is caused by a stretch injury to the brachial plexus (BRAY-key-el PLEK-sis). The brachial plexus is a network of nerves near the neck that give rise to all the nerves of the arm. These nerves provide movement and feeling to the arm, hand, and fingers.

One or two of every 1,000 babies have this condition. Most infants with brachial plexus birth palsy will recover both movement and feeling in the affected arm. Parents must be watchful and active participants in the treatment process to ensure maximum functional recovery.

 

The brachial plexus is formed as the nerves to the arm, hand, and fingers pass from the spinal cord between the bones (vertebrae) of the neck and go into the arm. Along the side of neck, these nerves merge together. From there, they branch out to form a “highway system,” or “plexus,” of nerves.

This system of nerves then travels below the collarbone (clavicle) and spreads out into the arm. The nerves that go to the shoulder lie higher in the neck than those that travel to the hand and fingers. Nerves that provide feeling to the hand and fingers lie lower in the neck, just above the chest.

There are many nerves in the brachial plexus. Each nerve contains many little nerve fibers with layers of “insulating” tissue.

Cause

Brachial plexus stretch injuries iewborns usually occur during a difficult delivery, such as with a large baby, a breech presentation, or a prolonged labor. It may also happen when the person assisting the delivery must deliver the baby quickly and exert some force to pull the baby from the birth canal. If one side of the baby’s neck is stretched severely, the nerves may also be stretched, causing the injury.

Most often, it is the upper nerves that are affected. This brachial plexus birth palsy is known as Erb’s palsy. The infant may not be able to move the arm, but may be able to move the fingers. If both the upper and lower nerves are stretched, the condition is usually more severe than just Erb’s palsy. This is called a “global,” or total, brachial plexus birth palsy.

Symptoms

In general, there are four types of nerve injuries. One infant may have one or more types of injury.

A stretch injury that “shocks,” but does not tear, the nerve is the most common type. This is called a neurapraxia (new-rah-PRAK-see-ah). Normally, these injuries heal on their own, usually within three months. Neurapraxia is not limited to infants. It can happen in adults as well. For example, when it happens to football players who are injured during play, they call this ‘”burners and stingers.”

A stretch injury that damages some of the nerve fibers may result in scar tissue. This scar tissue presses on the remaining healthy nerve. This condition is called a “neuroma.” Some, but not total, recovery usually occurs.

A stretch injury that causes the nerve to be torn apart (ruptured) will not heal on its own. A rupture happens when the nerve itself is torn.

The fourth type of injury, an “avulsion,” happens when the nerve is torn from the spinal cord. Nerve ruptures and avulsions are the most serious types of nerve injury. It may be possible to repair a rupture by “splicing” a donor nerve graft from another nerve of the child. It is not possible to repair an avulsion from the spinal cord. In some cases, it may be possible to restore some function in the arm by using a nerve from another muscle as a donor.

The symptoms of a nerve injury (loss of feeling and partial or complete paralysis) are the same, regardless of the type of injury. It is the severity of the injury that affects both treatment decisions and the extent of recovery possible.

 

A pediatrician will usually be the one to make the diagnosis of a brachial plexus palsy injury, based on weakness of the arm and physical examination. A doctor may order an X-ray or other imaging study to learn whether there is any damage to the bones and joints of the neck and shoulder. The doctor may also do some tests to learn whether any nerve signals are present in the muscle of the upper arm. These tests may include an electromyogram (EMG) or a nerve conduction study (NCS).

Because most newborns with brachial plexus birth palsy recover on their own, the baby will be re-examined frequently to see if the nerves are recovering. It may take up to two years for complete recovery. During this time, the parent will be taught how to do exercises with the baby to protect the soft joints and to keep the baby’s arm in good condition.

Sometimes, the affected arm is noticeably smaller than the unaffected arm. This occurs, in part, because the arm is not used as much. This also occurs because normal nerves do have an effect on growth. Although the size difference is permanent, the arm will still grow until the child stops growing.

Nonsurgical Treatment

Because a baby cannot move the affected arm alone, it is important that parents take an active part in keeping the joints limber and the functioning muscles fit. Daily physical therapy and range of motion exercises, done as often as possible during the day, begin when the baby is about three weeks old. The exercises will maintain the range of motion in the shoulder, elbow, wrist, and hand. This will prevent the joint from becoming permanently stiff, a condition called a joint contracture.

Surgical Treatment

 

If there is no change over the first three to six months, the doctor may discuss exploratory surgery on the nerves to improve the potential outcome (prognosis). Nerve surgery will not restore normal function, and is usually not helpful for older infants. Because nerves recover very slowly, it may take several months, or even years, for nerves repaired at the neck to reach the muscles of the lower arm and hand.

Many children with brachial plexus injuries will continue to have some weakness in the shoulder, arm, or hand. There may be surgical procedures that can be performed at a later date that might improve function.

The doctor will discuss the various treatment options and make a specific recommendation based on each child’s individual situation. Do not hesitate to ask questions. There is much that parents can do to help ensure a good return of function.

Children are very adaptable. Parents should be supportive and encouraging, focusing on what the child can do. This will help a child develop a healthy sense of self-esteem and compensate for any limitations in function.

 

 CRANIAL NERVE AND SPINAL CORD INJURY Cranial nerve and spinal cord injuries result from hyperextension, traction, and overstretching with simultaneous rotation. They may range from localized neurapraxia to complete nerve or cord transection.

Cranial nerve injury

Unilateral branches of the facial nerve and vagus nerve, in the form of recurrent laryngeal nerve, are most commonly involved in cranial nerve injuries and result in temporary or permanent paralysis.

Compression by the forceps blade has been implicated in some facial nerve injury, but most facial nerve palsy is unrelated to trauma.

 

Physical findings for central nerve injuries are asymmetric facies with crying. The mouth is drawn towards the normal side, wrinkles are deeper on the normal side, and movement of the forehead and eyelid is unaffected. The paralyzed side is smooth with a swollen appearance; the nasolabial fold is absent; and the corner of the mouth droops. No evidence of trauma is present on the face.

Physical findings for peripheral nerve injuries are asymmetric facies with crying. Sometimes evidence of forceps marks is present. With peripheral nerve branch injury, the paralysis is limited to the forehead, eye, or mouth.

The differential diagnosis includes nuclear genesis (Möbius syndrome), congenital absence of the facial muscles, unilateral absence of the orbicularis oris muscle, and intracranial hemorrhage.

Most infants begin to recover in the first week, but full resolution may take several months. Palsy that is due to trauma usually resolves or improves, whereas palsy that persists is often due to absence of the nerve.

Management consists of protecting the open eye with patches and synthetic tears (methylcellulose drops) every 4 hours. Consultation with a neurologist and a surgeon should be sought if no improvement is observed in 7-10 days.

Diaphragmatic paralysis secondary to traumatic injury to the cervical nerve roots supplying the phrenic nerve can occur as an isolated finding or in association with brachial plexus injury. The clinical syndrome is variable. The course is biphasic; initially the infant experiences respiratory distress with tachypnea and blood gases suggestive of hypoventilation (ie, hypoxemia, hypercapnia, acidosis). Over the next several days, the infant may improve with oxygen and varying degrees of ventilatory support. Elevated hemidiaphragm may not be observed in the early stages. Approximately 80% of lesions involve the right side and about 10% are bilateral.

The diagnosis is established by ultrasonography or fluoroscopy of the chest, which reveals the elevated hemidiaphragm with paradoxic movement of the affected side with breathing.

The mortality rate for unilateral lesions is approximately 10-15%. Most patients recover in the first 6-12 months. An outcome for bilateral lesions is poorer. The mortality rate approaches 50%, and prolonged ventilatory support may be necessary.

Management consists of careful surveillance of respiratory status, and intervention, when appropriate, is critical.

Laryngeal nerve injury

Disturbance of laryngeal nerve function may affect swallowing and breathing. Laryngeal nerve injury appears to result from an intrauterine posture in which the head is rotated and flexed laterally. During delivery, similar head movement, when marked, may injure the laryngeal nerve, accounting for approximately 10% of cases of vocal cord paralysis attributed to birth trauma. The infant presents with a hoarse cry or respiratory stridor, most often caused by unilateral laryngeal nerve paralysis. Swallowing may be affected if the superior branch is involved. Bilateral paralysis may be caused by trauma to both laryngeal nerves or, more commonly, by a CNS injury such as hypoxia or hemorrhage involving the brain stem. Patients with bilateral paralysis often present with severe respiratory distress or asphyxia.

Direct laryngoscopic examination is necessary to make the diagnosis and to distinguish vocal cord paralysis from other causes of respiratory distress and stridor in the newborn. Differentiate from other rare etiologies, such as cardiovascular or CNS malformations or a mediastinal tumor.

Paralysis often resolves in 4-6 weeks, although recovery may take as long as 6-12 months in severe cases. Treatment is symptomatic. Small frequent feeds, once the neonate is stable, minimize the risk of aspiration. Infants with bilateral involvement may require gavage feeding and tracheotomy.

Spinal cord injury

Spinal cord injury incurred during delivery results from excessive traction or rotation. Traction is more important in breech deliveries (minority of cases), and torsion is more significant in vertex deliveries. True incidence is difficult to determine. The lower cervical and upper thoracic region for breech delivery and the upper and midcervical region for vertex delivery are the major sites of injury.

Major neuropathologic changes consist of acute lesions, which are hemorrhages, especially epidural, intraspinal, and edema. Hemorrhagic lesions are associated with varying degrees of stretching, laceration, and disruption or total transaction. Occasionally, the dura may be torn, and rarely, the vertebral fractures or dislocations may be observed.

The clinical presentation is stillbirth or rapid neonatal death with failure to establish adequate respiratory function, especially in cases involving the upper cervical cord or lower brain stem. Severe respiratory failure may be obscured by mechanical ventilation and may cause ethical issues later. The infant may survive with weakness and hypotonia, and the true etiology may not be recognized. A neuromuscular disorder or transient hypoxic ischemic encephalopathy may be considered. Most infants later develop spasticity that may be mistaken for cerebral palsy.

Prevention is the most important aspect of medical care. Obstetric management of breech deliveries, instrumental deliveries, and pharmacologic augmentation of labor must be appropriate. Occasionally, injury may be sustained in utero.

The diagnosis is made by MRI or CT myelography. Little evidence indicates that laminectomy or decompression has anything to offer. A potential role for methylprednisolone exists. Supportive therapy is important.

BONE INJURY Fractures are most often observed following breech delivery and/or shoulder dystopia in macrosomia infants.

Clavicular fracture

The clavicle is the most frequently fractured bone in the neonate during birth and most often is an unpredictable unavoidable complication of normal birth. Some correlation with birth weight, midforceps delivery, and shoulder dystocia exists. The infant may present with pseudoparalysis. Examination may reveal crepitus, palpable bony irregularity, and sternocleidomastoid muscle spasm. Radiographic studies confirm the fracture.

Healing usually occurs in 7-10 days. Arm motion may be limited by pinning the infant’s sleeve to the shirt. Assess other associated injury to the spine, brachial plexus, or humerus.

Long bone fracture

Loss of spontaneous arm or leg movement is an early sign of long bone fracture, followed by swelling and pain on passive movement. The obstetrician may feel or hear a snap of fracture at the time of delivery. Radiographic studies of the limb confirm the diagnosis.

Femoral and humeral shaft fractures are treated with splinting. Closed reduction and casting is necessary only when displaced. Watch for evidence of radial nerve injury with humeral fracture. Callus formation occurs, and complete recovery is expected in 2-4 weeks. In 8-10 days, the callus formation is sufficient to discontinue immobilization. Orthopedic consultation is recommended.

Radiographic studies distinguish this condition from septic arthritis.

Epiphysial displacement

Separation of humeral or femoral epiphysis occurs through the hypertrophied layer of cartilage cells in the epiphysis. The diagnosis is made clinically based on the finding of swelling around the shoulder, crepitus, and pain when the shoulder is moved. Motion is painful, and the arm lies limp by the side. Because the proximal humeral epiphysis is not ossified at birth, it is not visible on radiography. Callus appears in 8-10 days and is visible on radiography.

Management consists of immobilizing the arm for 8-10 days. Fracture of the distal epiphysis is more likely to have a significant residual deformity than is fracture of the proximal humeral epiphysis.

INTRA-ABDOMINAL INJURY Intra-abdominal injury is relatively uncommon and can sometimes be overlooked as a cause of death in the newborn. Hemorrhage is the most serious acute complication, and the liver is the most commonly damaged internal organ.

Signs and symptoms of intraperitoneal bleed

Bleeding may be fulminant or insidious, but patients ultimately present with circulatory collapse. Intra-abdominal bleeding should be considered for every infant presenting with shock, pallor, unexplained anemia, and abdominal distension. Overlying abdominal skin may have bluish discoloration. Radiographic findings are not diagnostic but may suggest free peritoneal fluid. Paracentesis is the procedure of choice.

Hepatic rupture

The most common lesion is subcapsular hematoma, which increases to 4-5 cm before rupturing. Symptoms of shock may be delayed. Lacerations are less common, often caused by abnormal pull on peritoneal support ligaments or effect of excessive pressure by the costal margin. Infants with hepatomegaly may be at higher risk. Other predisposing factors include prematurity, postmaturity, coagulation disorders, and asphyxia. In cases associated with asphyxia, vigorous resuscitative effort (often by unusual methods) is the culprit. Splenic rupture is at least a fifth as common as liver laceration. Predisposing factors and mechanisms of injury are similar.

Rapid identification and stabilization of the infant are the keys to management, along with assessment of coagulation defect. Blood transfusion is the most urgent initial step. Persistent coagulopathy may be treated with fresh frozen plasma, transfusion of platelets, and other measures.

Hepatic rupture has no specific racial predilection and has equal sex distribution. Patients usually present immediately following birth, or rupture becomes obvious within the first few hours or days.

TRAUMA

Questions and answers about birth trauma

28-1 WHAT IS TRAUMA?

Trauma means damage or injury. During delivery the infant may be damaged by pressure on the body as it passes down the birth canal. The infant may also be damaged by the person conducting the delivery, either during a vaginal birth or caesarean section..

28-2 WHICH INFANTS ARE AT AN INCREASED RISK OF TRAUMA?

1. PRETERM INFANTS who have delicate tissues that are easily damaged.

2. LARGE INFANTS where there is difficulty delivering the head and shoulders.

3. MALPRESENTATIONS, e.g. breech delivery where the infant has to be manipulated.

4. FORCEPS OR VACUUM DELIVERY where traction or suction is applied to the head.

5. UNASSISTED DELIVERIES where the infant may fall after delivery.

6. PRECIPITOUS DELIVERIES when the infant is delivered very fast.

28-3 WHAT ARE THE MAJOR TYPES OF TRAUMA?

1. Caput (i.e. caput succedaneum).

2. Cephalhaematoma.

3. Subaponeurotic haemorrhage.

4. Facial palsy.

5. Brachial palsy.

6. Bruising.

7. Fractures.

8. Lacerations.

28-4 WHAT IS CAPUT?

Caput (or caput succedaneum) is oedema of the presenting part caused by pressure on the presenting part during a vaginal delivery. It is usually of no clinical importance and disappears during the first 48 hours after delivery. You should explain this to the parents especially if the caput is large.

More severe caput, often with damage to the skin, may be present on the infant’s head after a vacuum extraction (when it is called a chignon) or on the buttocks after a breech delivery.

28-5 WHAT IS A CEPHALHAEMATOMA?

A cephalhaematoma is a collection of blood under the periosteum of the parietal bone. It is common, may be unilateral or bilateral, and appears within hours of delivery as a soft, fluctuant swelling on the side of the head. A cephalhaematoma never extends beyond the edges of the bone and, therefore, never crosses suture lines.

Bleeding is caused by damage to capillaries under the periosteum of the parietal bone. This may occur during a normal vaginal delivery, but is more common with cephalopelvic disproportion or an assisted delivery.

28-6 WHAT IS THE TREATMENT OF A CEPHALHAEMATOMA?

Cephalhaematomas are usually small and need no treatment. The reabsorption of blood may cause jaundice, however, which may require treatment by phototherapy. It can take up to 3 months before the cephalhaematoma disappears. A bony ridge may form at the edge of the healing haematoma but this also eventually disappears without treatment.

28-7 WHAT IS A SUBAPONEUROTIC HAEMORRHAGE?

A subaponeurotic haemorrhage is a collection of blood under the aponeurosis of the scalp. The aponeurosis is a sheet of fibrous tissue connecting the muscle over the forehead with that over the occiput (back of the head). The subaponeurotic space is large and can contain a lot of blood.

Fortunately a subaponeurotic haemorrhage is not common.

A subaponeurotic haemorrhage results from trauma to blood vessels crossing this space from the skull to the overlying scalp. It is almost always caused by a forceps delivery or vacuum extraction.

A subaponeurotic haemorrhage presents with:

1. SHOCK AND PALLOR. Shock presents with tachycardia, a low blood pressure and delayed capillary filling time. Within 30 minutes of the haemorrhage the haemoglobin and packed cell volume start to fall rapidly. There is a great danger that the infant will die of blood loss.

2. A BOGGY SWELLING OF THE HEAD. As the subaponeurotic space crosses the sutures, the blood is able to track over the whole head. A subaponeurotic haemorrhage gives a diffuse swelling of the head in contrast to the localised swelling in a cephalhaematoma. Sutures usually are not palpable. The amount of blood under the scalp is far more than is estimated. Within 48 hours the blood tracks between the fibres of the occipital and frontal muscles causing bruising

behind the ears, along the posterior hair line and around the eyes.

IT IS IMPORTANT TO DIFFERENTIATE BETWEEN CAPUT, A CEPHALHAEMATOMA AND A

SUBAPONEUROTIC HAEMORRHAGE

28-8 WHAT IS THE TREATMENT OF A SUBAPONEUROTIC HAEMORRHAGE?

The treatment consists of transfusing the infant with blood to replace the blood which has been lost. Into the subaponeurotic space While waiting for the blood to arrive, transfuse with normal saline (or stabilized human serum or fresh frozen plasma, HAEMACCEL or PLASMOLYTE B) to correct the shock.

Give Konakion 1 mg by intramuscular or intravenous injection to assist the liver to replace clotting factors which are lost with the haemorrhage.

A SUBAPONEUROTIC HAEMORRHAGE REQUIRES EMERGENCY TREATMENT TO REPLACE

THE BLOOD LOSS

*** A subdural haemorrhage is a collection of blood in the subdural space. Severe moulding and marked traction on the head during delivery causes a tear in the large veins and sinuses draining blood from the brain. These vessels then bleed into the subdural space. A subdural haemorrhage is uncommon and is usually seen after a difficult forceps delivery or vacuum extraction in a woman with

cephalopelvic disproportion. This form of trauma should be prevented.

A subdural haemorrhage presents with:

(i) Shock and/or anaemia due to blood loss.

(ii) Neurological signs due to brain compression, e.g. convulsions, apnoea, a dilated pupil or a depressed level of consciousness.

(iii) A full fontanelle and splayed sutures due to raised intracranial pressure.

The infant may die of blood loss or brain compression. Management consists of replacing the blood lost and transferring the infant urgently to the nearest level 2 or 3 hospital where the subdural haemorrhage

may needed to be drained.

28-9 WHAT IS A FACIAL PALSY?

Facial palsy is muscle weakness of one side of the face due to trauma to the facial nerve. This is almost always caused by pressure from a forceps blade on the facial nerve just in front of the ear.

The affected side of the face droops and the infant is unable to close the eye tightly on that side. When crying the mouth is pulled across to the normal side. Fortunately the weakness usually recovers spontaneously in a few days or weeks and no treatment is needed.

FACIAL PALSIES USUALLY RECOVER SPONTANEOUSLY WITHIN DAYS OF DELIVERY

*** The asymmetric crying face syndrome mimics a facial palsy but the infant is able to close the eye on the weak side. Usually the weakness of the face is only seen when the infant cries and the mouth is pulled to the normal side. The weakness is due to congenital absence of the muscles on one side of the

face and does not improve with time.

28-10 WHAT IS A BRACHIAL PALSY?

Brachial palsy (or Erb’s palsy) is usually caused by excessive traction on the head and neck during a difficult vertex delivery. The infant is usually large and born at term with difficulty in delivering the shoulders. Brachial palsy may also complicate a poorly managed breech delivery. By stretching the neck, the brachial plexus of nerves is stretched and damaged.

Immediately after birth it is noticed that the infant does not move one arm due to weakness at the shoulder and elbow. The arm is fully extended, rotated inwards and held beside the body (the porter’s tip position). Movement of the hand and fingers is normal, however. The infant also has a markedly asymmetrical Moro reflex. Unless there is an associated fracture, there is no tenderness, pain or

swelling of the arm.

A BRACHIAL PALSY MAY RESULT IN PERMANENT WEAKNESS OF THE ARM

28-11 WHAT IS THE TREATMENT OF BRACHIAL PALSY?

Usually the weakness is much better by a week and full movement and power return. If the nerves in the neck have been torn, however, the infant will still not be able to flex the elbow after a week and some weakness will remain permanently. There is little hope of spontaneous recovery if the arm is not better

by 6 weeks.

Splints and keeping the arm above the head will not help recovery. Every time the nappy is changed however, the arm should be put through a full range of movements to prevent the development of contractures. If weakness remains by 6 weeks, the infant must be referred to a level 3 hospital for investigation and possible surgery to repair the torerves.

28-12 WHAT CAUSES BRUISING?

Bruising is common after difficult deliveries, especially breech delivery in a preterm infant. The bruise is due to bleeding into the skin and muscle caused by the rupture of small blood vessels. A tight umbilical cord around the neck commonly causes severe congestion and bruising of the face.

The bruise usually does not cause problems although the area may be tender for a few days. The bruise fades after a week or two and needs no treatment. The reabsorbed blood is converted into bilirubin and may cause jaundice, requiring phototherapy.

Bruising appearing after the first day is serious and suggests a bleeding problem or intentional (non accidental) trauma (battering).

28-13 WHAT FRACTURES ARE SEEN IN THE NEWBORN INFANT?

The clavicle is the bone most commonly fractured at birth. Fractures of the humerus, femur and skull are fortunately uncommon.

Fractures are usually caused by very difficult and traumatic deliveries. The fracture may be heard during delivery and bony crepitus (a grating feeling) may be felt after birth when the bone is palpated.

If the humerus or femur is fractured, the limb is usually swollen, tender and bruised. If the clavicle or humerus are broken, the infant will not move that arm, and will cry if the arm is moved. An asymmetric Moro reflex may mimic a brachial palsy. Fracture of a femur may cause shock due to blood loss. The

clinical diagnosis of a fracture can be confirmed by X-ray. Rarely the skull can be indented in a depressed fracture after a difficult delivery.

28-14 HOW ARE FRACTURES TREATED?

Fracture of the clavicle needs no treatment and heals well.

With fracture of the humerus, the arm should be immobilized to lessen the pain by strapping it to the side of the chest. A fractured femur is treated with gallows traction after the infant has been resuscitated. Paracetamol (Panado syrup 2,5 ml) should be given for pain relief in all fractures.

If a depressed fracture of the skull does not correct spontaneously in 24 hours, or if the infant develops neurological signs, it must be referred urgently for the skull to be surgically elevated.

28-15 WHAT IS THE MANAGEMENT OF LACERATIONS?

Lacerations are usually made during a caesarean section, when the infant is cut by mistake as the uterus is opened. The infant may also bleed after a fetal scalp blood sample has been taken. Small cuts can be held closed with strapping. Large cuts must be sutured as soon as possible after delivery.

 

Prophylaxis of birth injuries           

Sanation and treatment of pregnant woman.

Adequate management of the delivery 

Consequences of birth injuries           

·                   Paralyses and pareses

·                   Cerebral palsy

·                   Epilepsy

·                   Hydrocephalus

·                   Oligofrenia

CONCLUSION Recognition of trauma necessitates a careful physical and neurologic evaluation of the infant to establish whether additional injuries exist. Occasionally, injury may result from resuscitation. Symmetry of structure and function should be assessed as well as specifics such as cranial nerve examination, individual joint range of motion, and scalp/skull integrity.

Electronic fetal monitoring (“EFM”) is a diagnostic tool used to identify a fetus at risk for neurological injury or death, so that timely and appropriate intervention can be carried out before the underlying condition causes irreversible damage. Clinicians use EFM to perform fetal heart rate (“FHR“) testing to assess fetal well-being during labor and delivery, when high risk factors exist, or when specific clinical conditions develop before labor and delivery that place the fetus at risk for irreversible brain damage or death.

The goal of FHR monitoring is to detect fetal hypoxia at its earliest stage, and to attempt to prevent asphyxia resulting from prolonged and severe hypoxia. EFM can help to attain this goal because the effects of hypoxia and ischemia on the central nervous system (“CNS”) can produce abnormal FHR patterns that can be associated with fetal distress. For FHR testing to have a predictive value, however, the person interpreting the test results should be capable of properly interpreting FHR patterns, recognizing nonreassuring and potentially ominous signs, and intervening before brain damage or fetal death occurs. The sooner that the clinician intervenes, the higher the probability of avoiding irreversible brain damage.

An understanding of the following concepts is critical:

Baseline:  The baseline rate is the rate that persists over a given period of time. The interval is typically more than ten minutes. Normal baseline is 120-160 beats per minute (“bpm”). Baseline above 160 bpm is called a Tachycardia. Baseline below 110-120 bpm is called a Bradycardia.

Periodic Changes:  Periodic changes are FHR accelerations or decelerations that occur with contractions. Decelerations are routinely described as early, late, or variable.

Early Decels:  Early decelerations have a gradual drop in the FHR with the onset of the drop occurring with the onset of a contraction. The U-shape of the early decel mirrors the 1-shape of the contraction. An early decel is not associated with acidosis, but is the result of head compression or parasympathetic stimulation. Early decelerations are not associated with fetal hypoxia, acidosis, or low Apgar scores.

Late Decels:  Late decelerations have the same characteristics as early decels, but the onset occurs after the onset of the contraction. Late decelerations are associated with uteroplacental insufficiency. The size and depth of a late decel is not the key, because even subtle late decels can be ominous. As the contraction builds, blood flow through the placenta is diminished, leaving the fetus to rely on reserves. When reserves are inadequate, the FHR decreases and a late decel occurs. After the contraction ends, normal blood flow usually resumes and the FHR recovers.

Variable Decels:  Variable decels can occur before, during, or after a contraction, or wheo contraction is present (nonperiodic). It is characterized by an abrupt drop in FHR, followed by an abrupt return to baseline. Variable decels can vary in size, timing, depth and duration. Also, atypical variable decelerations can occur, which are more diagnostic of a fetus at risk.

Variable decelerations are associated with cord compression. Thus, the duration of the decel may be tied to the period of time that the cord is compressed. When the umbilical cord is compressed, it causes an increase in fetal blood pressure, reduces oxygen supply to the fetus, and activates responses in the CNS which result in a decrease in FHR and the development of variable decelerations. As hypoxia becomes prolonged, the decelerations may become deeper and last longer.

Variability:  The fetal heart rate varies from one beat to the next, because two branches of the CNS control changes in the FHR. The sympathetic division is constantly trying to increase the FHR, while the parasympathetic division is trying to counteract this by slowing the FHR. These beat-to-beat changes are referred to as variability. Normally, the sympathetic and parasympathetic nervous systems have equal opposite effects on the FHR, resulting in a consistent heart rate pattern. When the equilibrium is altered, accelerations and decelerations may occur. Further, the reduction or cessation of oxygen flow to the CNS can lead to a decrease or loss of variability. The connection between hypoxia and the loss of variability enables a physician or nurse who is interpreting a FHR pattern to identify possible signs of fetal distress. Variability is used to predict fetal status at a given point in time. As hypoxia continues and acidosis develops, long-term variability may decrease. Short-term variability may be difficult to determine without using a direct internal scalp electrode.

Nonperiodic Changes:  Nonperiodic changes can occur spontaneously, without contraction activity, and they are also described as accelerations or decelerations. For example, variable decelerations can appear during a nonstress test and they may be a sign of cord compression or oligohydramnios, both of which can have adverse effects on the fetus.

 

Intrauterine Asphyxia: Clinical Implications for Providers of Intrapartum Care

Advances in science and technology have allowed researchers to gain a better understanding of the pathophysiology leading to long-term neurologic damage in newborns. Intrapartum events are now known to be an infrequent cause of adverse neurologic outcome. Clinicians caring for women during labor must have an understanding of the pathophysiology of intrauterine asphyxia as well as an awareness of the capabilities and limitations of available intrapartum fetal assessment tools to diagnose intrauterine fetal asphyxia or predict neurologic outcome. This article reviews the physiology of acid-base balance and fetal gas exchange as well as the current scientific understanding of the role of intrauterine asphyxia in the pathophysiology of neonatal encephalopathy and cerebral palsy. Recommendations for care and documentation are included.

Cases involving neurologic injuries account for some of the largest payments for claims against providers of obstetric care, with some awards reaching higher than 40 million dollars per case. Similarly, costs related to these cases absorb 60% of malpractice premiums. A growing body of evidence, however, confirms findings by researchers in the 1980s that intrapartum events are an infrequent cause of adverse neurologic outcome. Despite these findings, the perception that events during labor and delivery are the primary cause of cerebral palsy and other neurologic dysfunction persists. Clinicians have inadvertently fueled this misperception by failing to use consistent criteria and physiologically accurate definitions to describe fetal oxygenation during labor and birth.

Clinicians must have an accurate definition of intrauterine asphyxia to help guide intrapartum fetal surveillance and labor management and to avoid perpetuating the notion that intrapartum asphyxia is a common event and a common cause of long-term neurologic dysfunction. To achieve this, it is necessary first to have an understanding of fetal respiratory physiology, hypoxemia in the fetus, and the role of hypoxemia in the pathogenesis of neurologic damage. In addition, clinicians must understand the abilities and limitations of current intrapartum surveillance techniques used to predict asphyxia and newborn tests used to diagnose asphyxia.

This article reviews the physiology of acid-base balance and fetal gas exchange as well as current understanding of the role of intrauterine asphyxia in the pathophysiology of neonatal encephalopathy and cerebral palsy. The efficacy of intrapartum assessment modalities, such as fetal heart rate monitoring, fetal scalp stimulation, fetal scalp blood sampling, and cord gases in the identification of intrauterine asphyxia are discussed, and recommendations for clinical practice and documentation are outlined.

Several adaptive mechanisms facilitate transfer of gases between maternal and fetal circulation. The partial pressure of oxygen in maternal circulation is higher than in fetal circulation, which facilitates maternal-to-fetal transfer of oxygen via diffusion across the placental membranes. In addition, respiratory changes during pregnancy decrease the partial pressure of carbon dioxide (PCO₂) in maternal circulation; thus, the transfer of carbon dioxide from fetus to mother is facilitated. The fetus has adaptive mechanisms that support function and growth in a low-oxygen environment; fetal blood has more hemoglobin than adult blood, and fetal hemoglobin has a higher affinity for oxygen than maternal hemoglobin at the same partial pressures of oxygen. In addition, fetal circulation “overperfuses” certain organs such as the brain. Furthermore, relative to an adult, the fetus has an increased number of capillaries, increased cardiac output, and a higher As carbohydrates, fat, and proteins are metabolized in the cell to produce energy, hydrogen ions and carbon dioxide are released as waste products. Metabolism in the presence of oxygen is called aerobic metabolism. In this process, hydrogen ions combine with oxygen to form water, and carbon dioxide combines with water to form carbonic acid. In adults, carbonic acid is transformed back into carbon dioxide in the lungs and excreted on exhalation; thus, the lungs are the main regulator of acid-base balance in the body. The fetus, however, depends on maternal and placental circulation for the delivery of oxygen and the removal of the waste products of metabolism, including carbon dioxide.

In the absence of oxygen, cells can continue to produce energy, but this process, called anaerobic metabolism, cannot be maintained over the long term. When oxygen is not present to accept hydrogen ions, they form organic acids such as lactic acid. Buildup of organic acid changes the pH within the cells, and if this process continues too long, the pH will decrease to levels that result in cellular death. Normal adult cell function depends on the maintenance of a plasma pH within the range of 7.35 to 7.45 (slightly alkaline). Mean umbilical artery pH iewborns is between 7.25 and 7.30, indicating that cell function in the fetus can be maintained at a lower pH. Table 1 includes definitions of terms related to respiration and acid-base balance that are used in this article.

When carbon dioxide is not removed from circulation, there is a drop in blood pH as well. Any change in pH secondary to changes in the partial pressure of carbon dioxide (PCO₂) is termed a respiratory change. Therefore, a drop in blood values of pH resulting from an increase in the PCO₂ is classified as a respiratory acidemia. Similarly, if too much carbon dioxide is removed (e.g., during hyperventilation), hydrogen ion concentration may fall and cause an increase in blood pH. This is termed respiratory alkalemia.

The blood pH level is usually kept in balance via the interaction of nonvolatile acid with bicarbonate (HCO₃), which is produced by the kidneys. Any changes in pH due to changes in bicarbonate concentration are termed metabolic. If the production of lactic acid and other metabolic acids outstrips the body’s ability to produce enough bicarbonate as a buffer, a decrease in blood pH may result, creating a metabolic acidemia, which, if unimpeded, will progress to a drop in tissue pH (metabolic acidosis).

Asphyxia occurs when gas exchange is impaired enough to cause significant metabolic acidosis. As asphyxia progresses, the fetus loses the ability to protect vital organs. Eventually, there is a decrease in cardiac output. This, in turn, leads to marked hypotension and a subsequent further decrease in blood flow to the heart and the brain. Resultant central nervous system damage depends on a variety of factors, including duration and severity of compromised gas exchange, the underlying condition of the fetus, and the ability of noncirculatory mechanisms to protect brain cells and tissue from hypoxic injury and death. If prolonged and unrelieved, asphyxia will lead progressively to cellular death, tissue damage, organ and organ system failure, and, ultimately, fetal death.

Neonatal encephalopathy is “a clinically-defined syndrome of disturbed neurologic function” that is seen in the first days of life of a term or near-term infant, and is manifested by “difficulty with initiating and maintaining respirations, depression of tone and reflexes, subnormal level of consciousness, and often, seizures.” Neonatal encephalopathy that results from systemic hypoxemia and decreased cerebral perfusion leading to ischemia is termed hypoxic-ischemic encephalopathy. Neonatal encephalopathies, including hypoxic-ischemic encephalopathies, can have multiple etiologies, including metabolic disease, infection, drug exposure, trauma, genetic disorders, nervous system anomalies, and intrapartum asphyxia. Findings iear-term and term infants with hypoxic-ischemic encephalopathy include delay of spontaneous respirations at birth, seizures, altered level of consciousness, altered tone, decreased spontaneous movement, irregular respirations, apnea, poor or absent Moro’s reflex, abnormal cry and suck, altered papillary responses, and stupor that develop in the first 72 hours after birth. Long-term morbidity and/or mortality after hypoxic-ischemic encephalopathy depends on the extent and severity of the injury. However, not all hypoxic-ischemic encephalopathy results in permanent neurologic damage such as cerebral palsy.

Cerebral palsy is a term used to describe chronic, nonprogressive disorders appearing early in life, in which the defining symptoms are abnormal control of movement and posture. Cerebral palsy results from abnormal development of or damage to the regions of the brain that control posture and movement. Cerebral palsy types are classified by the number of limbs involved (e.g., hemiplegia, quadriplegia, or hemiparesis) and the type of movement disorder (e.g., spastic, athetoid/dyskinetic, akinetic, ataxic, or mixed). The incidence of cerebral palsy in the United States is approximately 1.0 to 2.3 per 1000 births.

Research suggests that spastic quadriplegia, and less often, dyskinetic cerebral palsy, are the only types of cerebral palsy associated with hypoxic intrapartum events but that neither of these types of cerebral palsy are specific to intrapartum asphyxia. However, hemiplegic cerebral palsy, spastic diplegia, and ataxia are not associated with intrapartum asphyxia in term infants.

Although intrauterine asphyxia is an established cause of neurologic damage, including cerebral palsy, determining the exact role of intrapartum asphyxia as a cause of permanent neurologic damage in a fetus is complicated. It is estimated that the overall incidence of neonatal encephalopathy attributable to intrapartum asphyxia alone (in the absence of antepartum abnormalities) is 1.6 per 10,000 births. Prematurity and infections during pregnancy both appear to be more common causes of cerebral palsy than intrapartum events. Infants weighing <1500 g at birth constitute approximately 25% of all cases of cerebral palsy. Several studies have demonstrated an association between chorioamnionitis and the development of cerebral palsy in the near-term and term fetus. Current evidence implicates inflammatory cytokines in the pathway that connects infection to subsequent neurologic damage.

Not only is causation of neurologic injury difficult to establish, but identifying the timing of the injury is also complicated. The proportion of cerebral palsy that may be attributed to intrapartum events is small and estimated to be between 3% and 20%.Because neonatal encephalopathy is an essential pathway to subsequent cerebral palsy, the role of preconceptional, antepartum, and intrapartum factors in the development of neonatal encephalopathy was investigated in a case-control study from western Australia. The authors examined infants born between 1993 and 1995. Multivariate analysis of 164 cases of neonatal encephalopathy revealed that 69% of the children with neonatal encephalopathy had only antepartum risk factors, 24% had both antepartum and intrapartum risk factors, and only 5% had intrapartum risk factors only (defined as the presence of an abnormal fetal heart rate tracing or abnormal fetal heart rate on auscultation and/or fresh meconium staining, or both, with an Apgar of <3 at 1 minute and an Apgar of <7 at 5 minutes). Two percent of the children had no identifiable perinatal risk factors.

includes selected factors associated with the development of neurologic dysfunction in the neonate. The low percentage of neonatal encephalopathy and cerebral palsy cases that appear to be attributable to intrapartum events partially explains why the rate of cerebral palsy in term infants in the United States has remained nearly unchanged despite obstetric interventions and increased use of fetal heart rate monitoring in labor.

In the last decade, two major task forces have provided guidance on differentiating cases of neonatal encephalopathy and cerebral palsy that may be due to intrapartum events from those that are due to events predating labor. Both task forces have reviewed and evaluated the research available and solicited opinions and written contributions from leading clinicians and scientists. In 1999, the International Cerebral Palsy Task Force published its consensus statement. The following year, the American College of Obstetricians and Gynecologists (ACOG) convened the Task Force on Neonatal Encephalopathy and Cerebral Palsy, and their consensus statement was published in 2003. Both task forces published criteria needed to diagnose cerebral palsy as secondary to an acute intrapartum event, with slight differences, as noted in Table 3.

 

Table 3.  Criteria to Define an Acute Intrapartum Event Sufficient to Cause Cerebral Palsy International Cerebral Palsy Task Force (1999) ACOG Task force on Neonatal Encephalopathy and Cerebral Palsy (2003) Essential Criteria*

1.                              Evidence of a metabolic acidosis in intrapartum fetal, umbilical arterial cord, or very early neonatal blood samples (pH < 7.00 and base deficit ≥12 mmol/L)

2.                              Early onset of severe or moderate neonatal encephalopathy in infants ≥34 wk of gestation

3.                              Cerebral palsy of the spastic quadriplegic or dyskinetic type

Essential Criteria ^†

1.                              Evidence of a metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH < 7.00 and base deficit ≥12 mmol/L)

2.                              Early onset of severe or moderate neonatal encephalopathy in infants ≥34 wk of gestation

3.                              Cerebral palsy of the spastic quadriplegic or dyskinetic type

4.                              Exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions, or genetic disorders

Criteria that together suggest an intrapartum timing, but by themselves, are nonspecific ‡

1.                              A sentinel (signal) hypoxic event occurring immediately before or during labor

2.                              A sudden, rapid, and sustained deterioration of the fetal heart rate pattern usually following the hypoxic sentinel event where the pattern was previously normal

3.                              Apgar scores of 0-6 for longer than 5 min

4.                              Early evidence of multisystem involvement

5.                              Early imaging evidence of acute cerebral abnormality

Criteria that together suggest an intrapartum timing (within close proximity to labor and delivery e.g., 0-48 h), but by themselves, are nonspecific to asphyxial insults

1.                              A sentinel (signal) hypoxic event occurring immediately before or during labor

2.                              A sudden and sustained fetal bradycardia or the absence of fetal heart rate variability in the presence of persistent, late, or variable decelerations, usually after a hypoxic sentinel event when the pattern was previously normal.

3.                              Apgar score of 0-3 beyond 5 min

4.                              Onset of multisystem involvement within 72 h of birth

5.                              Early imaging study showing evidence of acute nonfocal cerebral abnormality

 

The criteria outlined by the task forces and presented in Table 3 offer no guidance for the clinician in predicting or detecting asphyxia in labor. Clinicians continue to be limited by use of technology with an imprecise ability to identify the development of asphyxia in the fetus.

Theoretically, variant fetal heart rate patterns either lead to fetal hypoxia or are responses to fetal hypoxia. Therefore, electronic fetal heart rate monitoring (EFM) should enable clinicians to detect the presence or potential development of asphyxia and allow intervention in time to prevent or reduce neurologic damage. However, the use of fetal heart rate patterns to predict subsequent neurologic damage, such as cerebral palsy, results in a 99% false-positive rate. This is due in part to the fact that permanent neurologic damage is a rare event, and variant fetal heart rate patterns are extremely common. Furthermore, interpretation of a fetal heart rate tracing is a subjective process. Many of the published studies assessing the impact of EFM were conducted at a time when EFM was a new technology and there were few, if any, standard clinical definitions for what constituted an abnormal fetal heart rate tracing. Researchers have found that individuals considered experts in interpretation of fetal heart rate patterns will agree on approximately 60% of normal patterns but only 25% of pathologic patterns.

In addition, even with standard definitions for fetal heart rate pattern type, the positive predictive value for acidemia in fetuses demonstrating “abnormal” fetal heart rate patterns is less than 50%. A meta-analysis of nine early studies of EFM showed that in a population monitored with EFM, as opposed to intermittent auscultation, there was a substantial increase in the rate of cesarean birth (OR 1.53; 95% CI 1.17-2.01) with no significant reduction in overall perinatal mortality (OR 0.87; 95% CI 0.57-1.33). Current evidence suggests that continuous EFM and intensive auscultation (one-on-one nurse listening through a contraction every 15 minutes in the first stage of labor and every 5 minutes in the second stage) are equivalent for the prevention of fetal death but that neither is an effective tool for the prevention of cerebral palsy.

Thirty years of experience with EFM, coupled with increased understanding of fetal heart rate physiology, has increased our understanding of fetal heart rate response to labor. More recent studies on fetal heart rate patterns and their relationship to neonatal outcomes have been able to detect an association between specific fetal heart rate patterns and an increase in the risk of compromised neonatal outcomes. Although they have not been able to prove that the association is etiologic, the remarkable consistency in findings from this work has provided evidence that the following specific patterns correlate with an increased incidence of metabolic acidemia and of adverse fetal outcomes: 1) minimal or absent variability for an hour or more as a solitary finding not due to a known, benign cause such as maternal medication; 2) recurrent late decelerations or repetitive moderate to severe variables and minimal or absent variability; 3) persistent tachycardia or bradycardia and minimal/absent variability; or 4) persistent or progressive bradycardia, particularly bradycardia below 80 beats per minute. Although many of the fetuses who exhibit these variant heart rate patterns will have no evidence of compromise at birth, the presence of these patterns warrants further investigation to determine fetal well-being (see below) and, when appropriate, intrauterine resuscitation and expedited delivery.

Despite the poor predictive value of variant fetal heart rate patterns, EFM does provide us with the ability to establish fetal well-being. A fetal heart rate pattern with normal rate, moderate variability, presence of accelerations, and absence of periodic decelerations correlates highly with absence of fetal acidemia.

In the term fetus, the presence of accelerations of 15 beats per minute lasting 15 seconds or more is an excellent indicator of the absence of acidemia. This is true whether the accelerations are spontaneous or induced through scalp stimulation or vibroacoustic stimulation. It must be kept in mind, however, that approximately 50% of fetuses without accelerations after stimulation will have a fetal scalp pH of >7.20.

Fetal scalp blood sampling is another method that has been used during labor to identify fetuses with acidemia, but this technique is technically difficult and invasive, and it requires personnel and equipment not available in many birth settings. Because it only determines the presence or absence of fetal acidemia at one moment in time, it is not useful in subsequent clinical management beyond a short period of time. Fetal scalp sampling is, therefore, becoming less common as a method to evaluate fetal oxygenation in labor.

In 2000, the Food and Drug Administration approved the marketing of a fetal oxygen saturation-monitoring system. This system has an optical sensor that is applied to the fetal cheek and connected to a fetal cardiac monitor. Proponents of pulse oximetry argue that it can be used to reduce the false-positive rate of nonreassuring fetal heart tracing and, therefore, reduce the rate of operative and instrumental interventions. ACOG, citing concerns about increasing medical costs without demonstrated improvement in outcomes, currently does not recommend the use of fetal pulse oximetry. This monitoring modality, they argue, is not currently more effective than other monitoring and, thus, represents an unnecessary expense. Further studies on fetal pulse oximetry are underway, and it is possible that in the future, this testing modality may be used as an adjunct to EFM and fetal scalp or vibroacoustic stimulation in the assessment of fetal well-being in labor.

 

 

 

References:

 

1.     Avery‘s neonatology: pathophysiology and management of the newborn / G. B. Avery, M. G. MacDonald, M. M. K. Seshia [et al.]. – 6th ed. – Philadelphia : Lippincott Williams and Wilkins, 2005. – 354 p.

2.     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.

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

4.     Volpe J. J. Neurology of the newborn / J. J. Volpe. – Philadelphia : Saunders, 2001. – 343 p.

 

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