LEARNING OBJECTIVES

2.1 Care of the Newborn

1. Define the terminologies related to the new-born such as low birth weight, VLBW
prematurity intrauterine growth retardation, infant mortality rates etc.
 Low birth weight: infants weighing 2,500g or less at birth
 Prematurity: the condition of an infant born viable but before its proper time (born after a
gestation period of less than 37 weeks).
 Intrauterine growth retardation (IUGR): the rate of foetal growth that is less than normal
for the population and for the growth potential of a specific infant. IUGR produces infants
who are SGA.
 Symmetric IUGR: brain and body growth are both limited
 Asymmetric IUGR: body growth is restricted to a much greater extent than head (and thus,
brain)
 Infant mortality rates: deaths occurring from birth to 12mos of age per 1,000 live births
 Small for Gestational Age (SGA): infants having a birth weight that is more than two
standard deviations below the mean or less than the 10 th percentile of a population-specific
birth weight vs. gestational age plot.
 Very low birth weight (VLBW): infants weighing less than 1,500g
 Extremely low birth weight (ELBW): infants weighing less than 1,000g
Gestational age (weeks)
Preterm <37weeks
Extremely preterm <28
Very preterm 280 – 316
Moderate preterm 320 – 366
Moderate preterm 340 – 366
Term 370 – 416
Early term 370 – 386
Full term 390 – 406
Late term 410-416
Post term ≥420
(≥294days from 1st day of LNMP)
Post dates
Primip >410
Multip >413

2. Know the causes and risk factors for low birth weight, prematurity and intra-
uterine growth retardation
 LBW is caused by preterm birth, IUGR or both factors
 Preterm birth causes include maternal diseases (severe preeclampsia requiring elective
delivery, PROM, uterine abnormalities, placental bleeding [abruption, previa],
multifoetus gestation, drug misuse, foetal distress, maternal chronic illness, and
infection [UTIs, pyelonephritis, chorioamnionitis, bacterial vaginosis, and upper/lower
genitourinary tract infection with Chlamydia trachomatis, Ureaplasma urealyticum,
Mycoplasma hominis, Gardnerella vaginalis])
 IUGR (asymmetric or symmetric) may be caused by chromosomal anomalies (trisomy
conditions), congenital infections (toxoplasmosis, rubella, CMV), dwarf syndromes,
drugs, smoking, maternal undernutrition, toxaemia, placental insufficiency, etc.
Factors affecting birth weight-gestational age distributions:
1. Socioeconomic factors that affect nutritional level and access to health care
2. Altitude
3. Incidence of environmental factors that affect birth weight (smoking)
4. Racial distribution
 Major causes of neonatal mortality are diseases associated with preterm birth and low
birth weight (LBW) and lethal congenital anomalies.
3. Describe common findings or observation of the parent in their newborn babies
which are physiological, don’t require any specific intervention, and only
explanation /counselling of the parents is required.
Normal
General Inspection:
Heart rate should range from 100-180 beats/min (120-
160 awake; 70-80 asleep)
An irregularly irregular HR (premature atrial
contractions) should resolve in the first days.
Respiratory rate: 30-60 breaths/min
Skin:
 bruising, petechiae (over presenting part
associated with prolonged/difficult delivery)
 meconium staining
 plethora (overoxygenated/overheated)
 Erythema neonatorum (blush to reddish)
 vernix caseosa (whitish, greasy, pasty
covering over skin)
 lanugo (fine hair in preterms)
 birthmarks (capillary hemangiomas,
Mongolian spot, milia, miliaria, Erythema
toxicum, pustular melanosis)
Head:
 Circumference (OCF) is normally 32-37cm
 AF (1-4cm) PF (<1cm)
 AF closes 9-12 mos, PF closes 2-4 mos
 Molding (temporary asymmetry with return
to normal within 1 week)
 Sutures freely moveable
 Caput succedaneum (diffuse oedematous
swelling)
Neck:
 (+) Rooting reflex
o Palpate sternocleidomastoid
o Palpate thyroid
Face:
 Note any obvious abnormalities
 Bruising from birth trauma (presenting part)
 Forceps marks
Eyes:
 Subconjuctival haemorrhages (from birth
process)
 Uncoordinated extraocular movements
(common)
 (+) Red reflex
Nose:
 Temporary deformities (utero compression)
 Examine shape/size
Ears:
 Malformation/malposition to note
 Visualise tympanic membranes
Mouth:
 Examine hard and soft palates
Abnormal
Bradychardia
Apnoea
Generalised cyanosis (desaturation of 5g of Hb)
Pallor (anaemia, birth asphyxia, shock)
Ductal pallor (associated with a PDA)
Plethora (suggests polycythaemia)
Widespread/progressive petechiae (coagulopathy)
Jaundice (≤24 hours)
Dry skin with peeling (postmature infants, congenital
syphilis/candidiasis)
Large AF (hypothyroidism, osteogenesis imperfect)
Small AF (hyperthyroidism, microcephaly)
Bulging AF (↑ ICP, meningitis, hydrocephalus)
Depressed AF (dehydration)
Cephalhaematoma (subperiosteal haemorrhage that
never crosses midline)
Subgaleal haematoma (subepicranial aponeurosis
haemorrhage)
Separated sutures (↑ICP)
Craniosynostosis (premature suture closure)
Short neck (Turner’s syndrome, Noonan’s, Klippel-
Feil syndrome)
Sternocleidomastoid haematoma
Thyroid enlargement
Thyroglossal duct cyst
Hypertelorism (eyes widely separated)
Low-set ears
Flat philtrum (Faetal alcohol syndrome)
Persistent irregular extraocular movements
Brushfield spots (Down’s syndrome)
Colobomas (congenital fissure of the eye)
Glaucoma (cloudy cornea)
Cataract
Tumour (retinoblastoma)
Bilateral/unilateral choanal atresia (nasal obstruction)
Purulent nasal discharge (congenital syphilis)
NB babies are obligate nose breathers
Low-set
Posteriorly rotated
Natal teeth
 Predecidious (to be removed to avoid
 Ranula (cystic swelling @ floor of mouth) aspiration)
 Epstein’s pearls (keratin-containing cysts  True deciduous (non-loose, with roots; not
along gum lines @ junction of hard/soft to be extracted)
palate) Cleft palate
 Mucocele (lesion 2° to salivary gland trauma) Lingual frenulum (tongue-tie; surgical tx.)
Frothy/copious saliva (esophageal atresia,
tracheoesophageal fistula)
Oral thrush (C. albicans whitsh patches on tongue,
gingiva, or buccal mucosa)
Chest: Asymmetric (tension pneumothorax)
 Symmetrical Tachypnoea, retractions, grunting (distressed)
 Breath sounds (R/L axilla) Absent BS (pneumothorax, atelectasis)
Bowel sounds (diaphragmatic hernia)
 Pectus excavatum
 Enlarged breasts (3-4cm due to maternal
estrogens)
 Supernumerary nipples (extra nipples)
Heart: VSD (loud, harsh, blowing pansystolic murmur @
 Observe for: HR, rhythm, heart sound lower left sternal border; most close by 1st year)
quality, presence of a mumur PDA (harsh, continuous, machinery-type @ second
left intercostal space by 2-3rd day of life)
Aorta Coarctation (systolic ejection, radiates down
sternum to apex and interscapular area)
Peripheral pulmonic stenosis (systolic murmur
bilaterally on ant. chest, axillae and back
Tetralogy of Fallot (loud, harsh, systolic/pansystolic
@ left sternal border with single S2)
ASD (soft, systolic ejection @ upper left sternal
border)
Abdomen: Omphalocoele (protrusion of intestines covered by
 Look for obvious defects peritoneum with central umbilicus)
 Listen for bowel sounds Gastroschisis (fissure of ventral wall with non-
periosteum covered intestines usually to the right of
 Feel for distention/tenderness/mass the umbilicus)
o Liver palpable 1-2cm below costal Scaphoid abdomen (diaphragmatic hernia)
margin Hepatomegaly (CHF, hepatitis, sepsis)
o Spleen tip at costal margin Splenomegaly (CMV or rubella infections, sepsis)
Kidney enlargement (polycystic disease, renal vein
thrombosis, hydronephrosis)
Umbilicus: Only 2 vessels (renal or genetic anomalies; Trisomy
 Normally 1 vein, 2 arteries 18)
 Translucent cord Single artery (IUGR, congenital anomaly, ↑ perinatal
mortality rate)
Oedema, discharge, redness (urachus [duct of
allantois], omphalitis)
Greenish-yellow cord (meconium staining 2° to foetal
distress)
4. Be familiar with & discuss 5 basic principles for generic care of new born namely,
namely (sugar, water, infection, colour, and temperature)
 Clean delivery and clean cord care should be ensured through policies and practices for
prevention, detection and control of nosocomial infections; in home deliveries by
strengthening standards of cleanliness by using disposable delivery kits. A complementary
strategy to reduce neonatal tetanus is immunizing pregnant women with tetanus toxoid.
(Addresses Risk of Infection Principle)
 Prevention and management of neonatal hypothermia and hyperthermia should be ensured
through simple measures such as a warm room for delivery, immediate drying of baby and
skin-to-skin contact with the mother to prevent loss of body warmth. Birth attendants and
families need proper instructions on how to rewarm babies that become hypothermic i.e.
rubbing, extra clothing, and breastfeeding. (Addresses Thermal Stability Principle)
  Breast-feeding should be started within an hour of birth. Feeding should be as frequent as
the baby demands, without prelacteal feeds or other fluids and food. Knowledge about the
importance of breast-feeding should be disseminated among families and communities as
well as health workers and managers. (Addresses Hydration + Glucose level Principle)
 Birth asphyxia should be recognised promptly and management should follow the basic
principles of resuscitation: aspiration of mouths and nostrils, end ventilation with positive
pressure. (Addresses Oxygenation Adequacy Principle)

5. Be able to recognize and form a management plan for sick neonates based on the 5
basic principles of newborn care. Discuss the commonest disease entity of each
organ / system e.g. congenital cyanotic heart disease for CVS
PRINCIPLES OF ESSENTIAL NEWBORN CARE
Resuscitate and maintain an airway
Air

Immediately following delivery, if the mother and baby’s condition allows it, baby can be put on the
Warmth mother’s abdomen for skin-to-skin contact while baby is being dried as the cord is cut.
o Thorough drying of the baby’s skin especially the head, which constitutes a large part of the
neonatal surface area
o Wet skin can result in a large amount of heat loss with seriously detrimental hypothermia
o The vernix, the cheesy material stuck on newborn skin made of dead skin, hair and secretions,
serves to conserve heat and protect delicate newborn skin from environmental stress.

Infants should be fed early and frequently to avoid hypoglycemia. The frequency, duration, and
Food volume of feeds will be dependent upon whether the infant is breastfed or receives formula. Each
feeding should be recorded, and if the infant is fed formula, the volume of feeding should also be
recorded.

Breastfeeding is recommended because of its increased benefits for both the infant and mother compared
with formula feeding,
o except when medically contraindicated, such as in infants with mothers with human
immunodeficiency viral (HIV) infection or in some cases of maternal drug abuse

Breast fed infants

o should be breastfed as soon as possible after delivery, preferably in the delivery room
o should receive 8-12 feeds per day during the newborn hospitalization
o rooming-in, skin-to-skin contact, frequent demand feedings in the early postpartum period,
and lactation support increase the rate of successful feeding

Formula fed healthy newborns

o should be offered standard 20 cal/oz iron containing formula.
o are fed on demand, but the duration between feedings should not exceed four hours.
o The volume of feedings should be at least 0.5 to 1 oz per feed during the first few days of life.

Prevention of INFECTIONS
Hygiene o Clean environment
o “5 cleans” of birthing process
 Clean hands
 Clean delivery
 Clean cord cut (using sterile instrument or new blade to cut umbilical
cord)
 Clean cord tie
 Clean cord stump
o Hand-washing for care-givers
o Strict asepsis
o No sharing
o No sharing of equipment, sheets, towels, medicines, syringes etc. among neonates
o Sharing increases chances of transmission significantly and should be avoided
o Counsel parents on importance of hygiene care at home

Ensure the newborn infant stay close to its mother, and mothers have open access to their newborn
Love infant if he or she requires special care
 6. Be able to calculate fluid and caloric requirements for normal and sick newborns.
 Full-term is 150ml/kg/hr by 7th day of life until the end of the neonatal period (28days) and then
to 120ml/kg/hr. Extra needs to be given in a hot environment.
 Pre-term (less than 36wks GA) is 180ml/kg/hr by 7 th day of life; they lose more fluids quicker
than term neonates.

7. Be able to clinically estimate the level jaundice in a newborn, common causes,

pathophysiology and manage appropriately.
Jaundice indicates a TSB of >4mg/dL (68μmol/L) with the level of jaundice correlating with
bilirubin level according to Kramer’s Rule:
 Jaundice above nipple line = reliably predicts Bilirubin <12mg/dL (205μmol/L)

Zone Distribution of Jaundice TSB level (mg/dL) Quick SBR Index (μmol/L)
1 Head and neck 6 100 (103)
2 Trunk to umbilicus 9 150 (154)
3 Trunk to knees 12 200 (205)
4 Wrists and ankles 15 250 (257)
5 Hands and feet >15 >250 (257)

8. Learn pathophysiology and the management of the meconium aspiration

syndrome.
- MAS is defined as respiratory distress in newborn infants born through meconium-stained
amniotic fluid (MSAF) whose symptoms cannot be otherwise explained.
- 2-10% of infants born through meconium-stained amniotic fluid (MSAF) develop MAS.

Pathophysiology
- Umbilical cord compression → hypoxia → gasping and intrauterine meconium passage
→ meconium aspiration → hypoxemia and acidosis.
- Meconium aspiration inhibits surfactant, obstructs the respiratory tract, and induces
pneumonitis.
Clinical findings
 History of meconium-stained amniotic fluid, or meconium staining of infant (nails
become stained after 6hrs, and vernix after 12-14hrs)
 SGA or postmature
 Respiratory distress (marked tachypnea, cyanosis, indrawing, grunting, nasal flaring)
 Barrel-shaped chest (↑ AP diameter due to overinflation)
 Rales and rhonchi upon auscultation
 Pneumothorax and pneumomediastinum in severe MAS

Diagnosis
 Evidence of meconium-stained amniotic fluid (MSAF) or infant
 Respiratory distress at birth or shortly after birth
 Characteristic chest x-ray findings: streaky, linear densities (similar in appearance to
transient tachypnea of the newborn). As the disease progresses, the lungs typically appear
hyperinflated with flattening of the diaphragms. Diffuse patchy densities may alternate
with areas of expansion.

Differential diagnosis

Transient tachypnea of the
newborn (TTN)
Infants with delayed
transition from fetal
circulation
Respiratory distress
syndrome (RDS)
Pneumonia
Congenital cyanotic heart
disease
Isolated air leaks (e.g.
pneumothorax)
- TTN causes respiratory distress in later preterm infants (34-
37weeks).
- MAS is seen most frequently in postmature infants
(>41weeks)
- Improve quickly in comparison to those with MAS
- RDS generally occurs in preterm infant.
- MAS usually occurs in postmature infants.
- Difficult to differentiate from MAS. Thus, infants with
presumed MAS are treated with antibiotics while awaiting
culture results.
- Differentiated from MAS by physical exam, chest x-ray,
and echocardiography
- Differentiated from MAS by history (absence of
meconium-stained amniotic fluid), and chest x-ray.

Prevention
 Prevention of fetal hypoxia (with continuous FHR monitoring)
 Prevention of postmature delivery
 If liquor is meconium-stained, delivery should be expedited to prevent further hypoxia
and gasping.
 Tracheal suctioning of residual meconium in nonvigorous (depressed) infants (i.e. absent
or depressed respirations, deceased muscle tone, or HR <100/min). Tracheal suction is
not recommended for vigorous infants.
 Observe infants with MSAF with signs of respiratory distress in neonatal intensive unit
for 4-6hrs to ensure they transition successfully.
Management
 Supplemental O2
 Ventilation (positive pressure ventilation (PPV) or high frequency oscillatory ventilation
(HFOV)).
 Surfactant
 Correct metabolic abnormality (e.g. hypoglycemia, acidosis)
 Treat any PPHN
 Empirical antibiotic therapy (ampicillin and gentamicin)
 Minimal handling to avoid agitation

 If baby is not vigorous (↓ respiratory effort, poor muscle tone, HR<100)

 Do not stimulate baby, immediately suction the trachea (below vocal cord via direct
laryngoscopy.
 Suction for no longer than 5seconds.

 No meconium retrieved: do not repeat intubation and suction

 Meconium retrieved with no bradycardia: reintubate & suction
 Meconium retrieved with bradycardia: use positive pressure ventilation, consider
suctioning later

 If baby is vigorous (good respiratory effort, crying, good muscle tone, HR>100)
 Do not intubate
 Clear secretions and meconium from mouth and nose with bulb syringe or large-bored
suction catheter.

9. Enumerate conditions leading to respiratory distress in a new born and discuss

pathophysiology and management of Hyaline Membrane disease.
- Respiratory distress is common immediately after birth, and is typically caused by abnormal respiratory function during
the transition from fetal to neonatal life.
- It is manifested by tachypnea, nasal flaring, intercostal or subcostal retractions, audible grunting, and cyanosis.
- Neonatal respiratory distress may be transient; however, persistent distress requires a rational diagnostic and therapeutic
approach to optimize outcome and minimize morbidity.

Pathogenesis
- The 3 most common respiratory disorders of perinatal transition are:
 Transient tachypnea of the newborn (TTN)
 Respiratory distress syndrome (RDS)
 Peristant pulmonary hypertension of the newborn (PPHN)

TRANSIENT TACHYPEA OF THE NEWBORN (TTN)

- Is a parenchymal lung disorder characterized by pulmonary edema resulting from delayed resorption and clearance of
fetal alveolar fluid.

Pathophysiology
- Due to delayed resorption of fetal lung fluid.

Delayed resorption of fetal lung fluid

↓
Fluid fills the air spaces and moves into the extra-alveolar interstitium
↓
Pools in perivascular tissues and interlobar fissures until it is cleared by lymphatic or vascular circulations
↓
Excess lung water results in ↓ pulmonary compliance, and ↑ airway resistance due to compression of small airways
↓
Continued perfusion of poorly ventilated alveoli
↓
Hypoxemia

Risk factors for TTN

 Premature infants
 Cesarean delivery without labour (mechanisms to reabsorb alveolar fluid have not been initiated)
 Infants of mothers with DM.
 Maternal asthma

Clinical features
 Onset: at time of birth, and within 2hrs after delivery.
 Mild – moderate TTN: symptomatic for 12 to 24 hours
 severe TTN: signs may persist as long as 72 hours

 Tachypnea (>60/min)
 Cyanosis
 ↑ work of breathing: nasal flaring, mild intercostal and subcostal retractions, expiratory grunting
 ↑ AP diameter of chest
 Clear breath sounds, without rales or rhonchi

Diagnosis – TTN is a clinical diagnosis

 Chest x-ray: ↑ lung volumes with flat diaphragms, mild cardiomegaly, prominent vascular markings in a sunburst
pattern originating at the hilum. Fluid often seen in interlobar fissures. Pleural effusion may be present.
 Arterial blood gases: mild-moderate hypoxemia, mild hypercapnia, resulting in respiratory acidosis.
 FBC and differentials are normal

Differential diagnosis
 Pneumonia, sepsis
 Cardiac disease
 TTN complicating respiratory distress syndrome in premature infants

Management
 TTN is a benign, self-limited condition, management is supportive:
 Supplemental O2 is provided by hood or nasal cannula to maintain oxygen saturation >90%.
 Maintain warmth
 Provide nutrition

 If tachypnea persists >4-6hrs, or if initial RBC and differential are abnormal, obtain a blood culture and begin antibiotic
coverage with ampicillin and gentamicin while awaiting the results
 Fluid restriction (40ml/kg for 1st day of life in term infants, 60ml/kg for 1st day of life in preterm infants)

RESPIRATORY DISTRESS SYNDROME (RDS) previously known as Hyaline Membrane disease.

- Is lung disease caused by surfactant* deficiency.
- Largely seen in preterm infants. Rare in >32weeks gestation.

 Surfactant: phospholipid mixture (predominantly desaturated palmitoyl phosphatidyl choline) synthesized by alveolar
type II cells, which reduces alveolar surface tension, which decreases the pressure needed to keep the alveoli inflated,
and maintains alveolar stability.

Etiology
 Surfactant deficiency
 Inability to clear lung fluid from air spaces
 Genetic susceptibility to RDS

Pathophysiology

 Surfactant deficiency
- Surfactant deficiency causes alveolar collapse, increased work of breathing, and hypoxia (due to intrapulmonary
shunting of blood):

 Surfactant deficiency → inability to maintain open alveoli → progressive and diffuse atelectasis (alveola
collapse) → low compliance and low functional residual capacity → ventilation-perfusion mismatch as blood
bypasses atelectic air spaces (intrapulmonary shunting) → hypoxemia.

- Right-to-left shunting that occurs through the ductus arteriosus and foramen ovale (due to increased pulmonary
vascular resistance (PVR)) also contributes to decreased oxygenation.
- Hypoxemia is often accompanied by respiratory and/or metabolic acidosis.

 Surfactant inactivation
 Due to meconium and blood aspiration

Associative risk factors

 Cesarean delivery
 Hypothermia
 Perinatal hypoxia
 Meconium aspiration
 Congenital pneumonia
 Maternal DM
 Past family history
Clinical manifestations (within 4hrs of birth)
 Tachypnea
 Nasal flaring
 Expiratory grunting (exhalation through partially closed glottis)
 Use of accessory respiratory muscles
 Indrawing (subcostal, intercostal, subxiphoid)
 Cyanosis (due to right-to-left intra- and extra-pulmonary shunting)

 ↓ breath sounds on auscultation

 ↓ peripheral pulses
 Low urine output
 Peripheral edema

Clinical course
- Prior to surfactant use, uncomplicated RDS typically progressed for 48-72 hrs.
- This was followed by an improvement in respiratory function (associated with increased production of endogenous
surfactant), and resolution of the respiratory disorder by 1 week of age.
- A marked diuresis typically preceded the improvement in lung function.

- The natural history of RDS is greatly modified by treatment with exogenous surfactant, which dramatically improves
pulmonary function, leading to the resolution of symptoms, and shortens the clinical course.
- In addition, the use of continuous positive airway pressure (CPAP) has also improved the clinical course of RDS, even
in infants who do not receive surfactant therapy.

Diagnosis
 Clinical diagnosis: premature infant with onset of progressive respiratory failure shortly after birth.
 Chest x-ray: bilateral, diffuse ‘ground-glass’ appearance (due generalized atelectasis contrasting with aerated airways),
airway bronchograms, reduced lung volume.
 Arterial blood gas measurements – typically show hypoxemia that responds to administration of supplemental O 2.
 Hyponatremia (as disease progresses – due to water retention).

PERSISTENT
PULMONARY

HYPERTENSION OF THE NEWBORN (PPHN)

- Occurs when pulmonary vascular resistance (PVR) remains abnormally elevated after birth, resulting in right-to-left
shunting of blood through fetal circulatory pathways (foramen ovale and ductus arteriosus), resulting in severe
hypoxemia.
- Occurs primarily in term or late preterm infants ≥34 weeks gestation.
- Caused by a combination of: underdevelopment, maldevelopment, or maladaptation of the pulmonary vascular bed.

Presentation
 Hypoxia
 Mild breathlessness
 Loud single 2nd heart sound
 Echocardiography shows ↑ pulmonary arterial pressure, large right to left shunt at level of foramen ovale and ductus
arteriosus.

Management
 Treat cause; minimal handling
 Optimize BP, pH, Hb, U&E, blood glucose
 Ventilate
 Inhaled nitric oxide (results in selective pulmonary vasodilation)

10. Discuss pathophysiology and management of Neonatal sepsis

Neonatal sepsis
- Neonatal sepsis is a clinical syndrome in an infant ≤28days, manifested by systemic signs of infection and/or isolation
of a bacterial pathogen from the blood stream.

Early-onset sepsis - Bloodstream infection at ≤72 hours of age, or

- Group B streptococcal disease infection with onset of symptoms through day 6 of life.
Late onset sepsis - Onset of symptoms after first days of life, ranging from an onset at ≥72hrs or ≥7days of age.

- When pathogenic organisms gain access into the blood, they cause:
 Infection without localization (septicemia)
 Localized to lungs (pneumonia)
 Localized to meninges (meningitis)

Pathogenesis

 Early-onset sepsis
 Vertical transmission by
ascending contaminated
amniotic fluid.
 During vaginal delivery from
bacteria colonizing or
infecting the mother's lower
genital tract.

 Late-onset sepsis
 Maternal vertical
transmission, resulting in
initial neonatal colonization
that evolves into later
infection.
 Horizontal transmission from
direct contact with care
providers or environmental
sources. Disruption of the
intact skin or mucosa, which
can be due to invasive procedures (eg, intravascular catheter), increases the risk of late-onset infection.

Note:
- Neonates are highly susceptible to infections due to:
 Decreased cellular immunity because of deficient PMNs in chemotaixis and killing capacity.
 Decreased humoral immunity because of having only some preformed immunoglobulin (acquired from placental
transfer).
 Deficient barrier function. Skin and mucous membranes are broken down easily.

Etiology
Clinical manifestations
 Fetal and neonatal distress during labour and delivery can be the earliest signs of neonatal sepsis (e.g. intrapartum fetal
tachycardia, meconium-stained amniotic fluid, low APGAR score).

 Bulging fontanelle
 Severe jaundice
 Signs of pneumonia
 Severe abdominal distention
 Umbilical redness extending to peri-umbilical skin
 Umbilicus draining pus
 Severe skin pustules
 Painful joints, joint swelling, reduced movement and irritability if these parts are handled
Evaluation

 Maternal and neonatal risk factors  Other treatment

 Intrapartum maternal temperature ≥38ºC  If infant is drowsy or unconscious, ensure that
 Delivery at <37 weeks gestation hypoglycemia is not present. If it is, give
 Chorioamnionitis 2ml/kg 10% glucose IV.
 5minute Apgar score ≤6  Treat convulsions with phenobarbital
 Evidence of fetal distress
 Maternal GBS colonization
 Membrane rupture ≥18 hours – risk of proven
sepsis increases 10-fold to 1 percent when
membranes are ruptured beyond 18 hours 

 Lab investigations
 FBC
 Blood culture
 Urine culture
 Lumbar puncture
 Chest x-ray in an infant with respiratory
distress

Management
 Admit to hospital
 Perform lumbar puncture and obtain blood cultures
if possible before starting antibiotics
 Newborns with any signs of serious bacterial
infection or sepsis: ampicillin (or penicillin) and
gentamicin.
 Risk of staphylococcus infection (extensive skin
pustules, abscesses, omphalitis in addition to signs
of sepsis): give cloxacillin (instead of penicillin)
and gentamicin.
 The most serious bacterial infections in newborns
should be treated with antibiotics for at least 7-
10days.
 In not improving in 2-3days, change the antibiotic
treatment, or refer the infant for further
management.

 Duration and response to therapy

- (+) cultures: antibiotics continued for 10days.
- (-) cultures: empirical therapy discontinued in
well-appearing infant after 48hrs.
 11. Discuss various conditions
causing Hypoglycemia in a new born and discuss its management.
Hypoglycemia
- Blood glucose: <3mmol/L (<54mg/dL).
- Blood glucose drops naturally in first few hours after birth before normalizing. Newborns have increased ability to utilize
ketones/lactate for energy.
- All infants should be encouraged to feed in 1st hour if well enough.

Risk groups for hypoglycemia

 Infants of diabetic mother
 <2500g or <3rd centile for weight
 Premature infants (<37/40 weeks gestation)
 Maternal β blockers
 Birth asphyxia

Causes

↓ glucose stores  Preterm

 IUGR
 LBW
 Inborn errors of metabolism (e.g. galactosemia)
↑ glucose  Sepsis
consumption  Hypothermia
 Perinatal hypoxia
 Polycythemia
 Hemolytic disease
 Seizures
Hyperinsulinism  Maternal DM
 Beckwith-Wiedemann syndrome (BWS)
 Pancreatic cell hyperplasia
 Transient
Miscellaneous  Maternal β blockers
 Tissued or malfunctioning IV infusion
Other rare  Fetal alcohol syndrome
 causes  Pituitary insufficiency
 Adrenal insufficiency

Presentation (signs are non-specific)

 Commonly asymptomatic
 Jitteriness and/or tremors
 Tachypnea or apnea
 Drowsiness
 Poor feeding
 Weak or high-pitched cry
 Seizures
 Cerebral irritability
 Hypotonia
 Macrosomia (if hyperinsulinemia)

Investigations (especially for at-risk infants)

 Blood glucose level (measured within 1st hour in all high risk infants) – a low glucose value result with Dextrostix
(glucometer) screening should be confirmed by lab measurement.
 Urinalysis for ketones, amino, and organic acids.
 Evaluate for other possible causes (e.g. sepsis) if symptoms do not resolve after normalization of blood glucose
concentration

Management
 Asymptomatic infants: oral feedings of breast milk or formula.
 Symptomatic infants with severe hypoglycemia (<25mg/dL): IV glucose infusion (5ml/kg of 10% glucose solution).
 12. Describe some common neonatal injuries that occur in a new born at the time of birth.
Birth injury is defined as the structural destruction or functional deterioration of the neonate’s body due to a
traumatic event at birth. Some of these injuries are avoidable when appropriate care is available and others are
part of the delivery process that can occur even when clinicians practice extreme caution. Amniocentesis and
intrauterine transfusions can cause injuries before birth, and these and any injuries that occur following neonatal
resuscitation procedures are not considered birth injuries.

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, although this is uncommon.
The resolving hematoma predisposes to hyperbilirubinemia. Rarely, cephalhematoma may be a focus of infection
that leads to meningitis or osteomyelitis. Linear skull fractures may underlie a cephalhematoma (5-20% of
cephalhematomas). Resolution occurs over weeks, occasionally with residual calcification.

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 a vacuum applied to the head at delivery. 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 calvaria; 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. In the
absence of shock or intracranial injury, the long-term prognosis is generally good.

Caput succedaneum
Caput succedaneum is a serosanguineous, 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 molding. Caput succedaneum does not usually
cause complications and usually resolves over the first few days. Management consists of observation only.

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 of these lesions uneventfully heal.

Brachial Plexus Injury

Peripheral nerve damage in the form of 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 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 include the following:
 Fractured clavicle (10%)
 Fractured humerus (10%)
 Subluxation of cervical spine (5%)
 Cervical cord injury (5-10%)
 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. The
grasp reflex is usually present. Five percent of patients have an accompanying (ipsilateral) phrenic nerve paresis.
Klumpke paralysis (C7-8, T1) is rare and results in weakness of the intrinsic muscles of the hand; the grasp reflex is
absent. If cervical sympathetic fibers of the first thoracic spinal nerve are involved, Horner syndrome is present.

Cranial Nerve 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.
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 from obstetric instrumentation (eg, forceps). The compression appears to occur as the head
passes by the sacrum.
Physical findings for central nerve injuries are asymmetrical 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 asymmetrical 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.

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, caused most often 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 central nervous system (CNS) injury, such as hypoxia or
hemorrhage, that involves the brain stem. Patients with bilateral paralysis often present with severe respiratory
distress or asphyxia.

Spinal Cord Injury

Spinal cord injury incurred during delivery results from excessive traction or rotation. Major neuropathologic
changes consist of acute lesions, which are hemorrhages, especially epidural lesions, intraspinal lesions, 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, 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 brainstem. Severe respiratory failure may be obscured
by mechanical ventilation and may cause ethical issues later.

Bone Injury
Fractures are most often observed following breech delivery, shoulder dystocia, or both in infants with excessive
birth weights.

Clavicular fracture
The clavicle is the most frequently fractured bone in the neonate during birth; this is most often an unpredictable,
unavoidable complication of normal birth. [13] Some correlation with birth weight, midforceps delivery, and shoulder
dystocia is recognized. [14] 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. In order to decrease pain, 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 at the time of delivery. Radiographic studies of the
limb confirm the diagnosis and distinguish this condition from septic arthritis.
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.

Epiphysial displacement
Separation of the humeral or femoral epiphysis occurs through the hypertrophied layer of cartilage cells in the
epiphysis. The diagnosis is clinically based on 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 who presents with shock, pallor, unexplained anemia, and
abdominal distension. Overlying abdominal skin may have a 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; they are often caused by an abnormal pull on the peritoneal
support ligaments or by the 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, a 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.