Neonatal emergency medicine

Normal Feeding

• >90% have regular suitable feeding schedule by 1 month of age
• Guide for botte fed infants is 2-4 ounces every 2-4 hours by end of first week of life
  • Breastfed infants prefer shorter intervals (1-3 hours)
• Intake adequate if appears content after feeds and gaining weight appropriately
• Should stop losing weight at day 5-7 and gain weight by days 12-14
  • Lose up to 12% of body weight in first 3-7 days
  • Gain 30g/day for first 30 days

Normal stools

• Breastfed infants can go 5-7 days without passing stool
• Colour only important if acholic or bloody
• Typically one per day to one per week range

Colic

• Paroxysm of crying for 3 hours per day or more for 3 days per week or more over a 3 week period causing significant parental distress
• 13% incidence
• Described as paroxysmal crying, flush face, circumoral pallor, tense abdomen, drawn up legs, cold feet and clenched fists
• Rare after 3-4 months of life
• Diagnosis of exclusion
• Rx: 
  • Change caretaking style (increased soothing, reduces external stimulation)
  • Change environment (background music, car rides)
  • Change feeding in refractory cases e.g. 1-week trial hypoallergenic formula
  • Assess caregiver stress
  • Reassurance of self-limiting nature

• Crying peaks around 6-8 weeks of age
• May last hours
• Usually improves by 3-4 months of age
• Non-pathological precipitants
  • Excessive tiredness
    • <16 hrs at birth; 15 hours at 2-3 months
  • Hunger
    • More likely if mother reports frequent feeds (<3 hourly), poor weight gain or inadequate milk supply

Colic DDx

• Cow milk/soy protein allergy
  • Both enter human breast milk
  • Suspect if vomiting, blood/mucous stools, poor weight gain, eczema/wheeze, significant feeding problems
  • Diagnosis made by exclusion of cow milk from maternal diet or extensively hydrolysed formula for 2 weeks
• GOR
  • No causal relationship
  • Silent reflux is an unlikely cause
  • If 4 or more vomits per day, feeding difficulties or poor weight gain consider GORD
  • Can be due to cow’s milk protein allergy
  • Anti-reflux medications not recommended for colic
• Lactose overload/malabsorption
  • Suspect if frothy stools and perianal excoriation
  • Dx by faecal reducing substances >0.5% and pH <5.0 + clinical response to lactose-free formula
  • May be functional lactose overload if feeding >3 hourly or frequently switching sides

Colic management

• Explain normal crying patterns
• Encourage use of feed/sleep/cry diary
• Educate re: signs of tiredness (frowning, clenched hands, crying, grizzling)
• Help parents deal with baby distress
  • Establish routine
  • Predictable settling for naps (quiet play, move to bedroom, wrap, brief cuddle)
  • Avoid excessive stimulation and excessive quiet
  • Darken bedroom for daytime sleeps
  • Baby massage/rocking/patting
  • Gentle music
  • Respond before baby becomes too worked up
  • Give parents respite each day from social network

• Assess maternal emotional state and mother-baby relationship
  • Invite mother to talk about stress of current situation
  • Screen for depression (Edinburgh Postnatal Depression Scale)
• Printed information
• Need f/u within days
• Options
  • Maternal and child health nurse
  • Local GP
  • General paediatrician
  • Unsettled babies clinic
  • Mother-baby day unit
  • Admission if at risk of NAI or parental exhaustion

Erythema toxicum neonatorum

• First days of life with small erythematous or yellow papules over whole body
• Not warm, tender or indurated
• Most common vesicular disease of neonates
• Sparing of palms/soles
• Self-resolving

Neonatal pustular skin disorders

• DDx
  • Erythema toxicum neonatorum
  • S. aureus, H. influenzae, Group B strep
  • Congenital neutropaenia (may be only clinical sign)
  • Eosinophilic pustular folliculitis of the scalp
• Note: Milia are not true vesicles (inclusion cysts)
  • Self-resolve also

Neonatal acne

• Small papules/pustules on face and upper trunk
• 2^nd or 3^rd week of life due to maternal hormones
• Resolves without treatment in weeks

The critically ill neonate

• Always airway/breathing are priorities
• Major DDx
  • Congenital heart disease
  • IEM
  • Congenital adrenal hyperplasia
  • ICH
  • Abdominal catastrophe

• Inborn errors of metabolism: 
  • Glucose, ketones, ammonia, blood gas, electrolytes to start
  • Dextrose-containing IV fluid is often sufficient initial therapy
• Congenital adrenal hyperplasia
  • Always look for signs of virilisation or ambiguous genitalia and/or hyperpigmentation
  • Hyponatraemia/hyperkalaemia should trigger suspicion
  • Hydrocortisone 12.5-25mg IV should be promptly delivered

• Intracranial haemorrhage e.g. NAI or birth trauma
  • Risk factors include no Vit K, traumatic vaginal delivery or carer suspicion
  • Always consider CT brain in critically unwell neonates
• Abdominal catastrophe
  • E.g. congenital malrotation
  • Shock, cardiorespiratory collapse and distended abdomen

Diaper rash

• Contact dermatitis
  • Prolonged exposure to irritants
  • Macular and erythematous with sharply demarcated edges
  • Treat with air drying and topical barrier ointment (e.g. zinc oxide)
• Candidal diaper dermatitis
  • Erythematous plaque with scalloped border and sharp edge with satellite lesions
  • Usually moist, intertriginous zones
  • Topical anticandidal agent (e.g. nystatin cream) with each diaper change
  • Zinc oxide overlying antifungal to prevent friction
• Consider bacterial superinfection
  • If blistering or peeling, consider staphylococcal scalded skin syndrome or toxic epidermal necrolysis

Oral candidiasis

• White and flaky over mucosal membranes
• Common in normal newborns and those on antibiotics
• Cannot be scraped off tongue with depressor
• May be painful
• Topical oral antifungal (nystatin) +/- anaesthetic gel for feeding

The irritable neonate

• DDx (Bold = emergent)
  • CNS – ICH, meningitis, elevated ICP
  • ENT – Nasal obstruction, corneal abrasion, ocular FB, otitis media, nasal congestion, oral thrush, stomatitis
  • Pulmonary – Pneumonia
  • Cardiac – SVT, CCF
  • GI – Volvulus, intussusception, incarcerated hernia, reflux, gastroenteritis, anal fissure, colic
  • GU – Testicular torsion, penile hair tourniquets, paraphimosis, UTI, diaper rash
  • MSK – Hair tourniquet, NAI, Injuries
  • Infectious – Sepsis, pneumonia, meningitis, URTI
  • Metabolic – Inborn errors of metabolism, hypoglycaemia, congenital adrenal hyperplasia

Noisy breathing and stridor

• Stertor – Noisy snoring-type breathing from nasopharynx
  • Usually benign but may indicate choanal stenosis
  • Inability to pass a small NG tube is diagnostic

Noisy breathing

• Stridor
  • May be inspiratory or expiratory
  • Commonest cause is laryngomalacia (decreases over first year of life and is worse with crying)
    • Naso-pharyngoscopy by ENT confirms diagnosis
  • Can be fixed obstruction anywhere in upper airway including webs, cysts, atresia, stenosis, clefts, haemangiomas, tracheomalacia or subglottic haemangioma
  • If accompanied by feeding difficulties: Vascular ring, laryngeal cleft or tracheo-oesophageal fistula
  • Stridor with hoarseness or weak cry suggests vocal cord paralysis
  • Infection is a very rare cause in neonates but may be suggested by fever

Apnoea and periodic breathing

• Apnoea is cessation of breathing for 20 seconds or less if associated with bradycardia, cyanosis or change in muscle tone
• Signifies critical illness, impending respiratory muscle fatigue and pending arrest
• If no obvious cause, assume sepsis

• Periodic breathing
  • Common in neonates lasting up to 20 seconds
  • Much less common with CNS maturity at 6mo
  • Requires careful history/exam and focused investigation for:
    • CNS disease (ICH, seizures, meningitis, NAI)
    • Early sepsis (exam, temps, septic screen)
    • Metabolic or electrolyte abnormality (BSL, UEC, VBG, ammonia)
    • Dehydration
    • Obvious respiratory causes can be ruled out by examination
    • Consider breastfeeding mother taking medications/drugs
  • Period of observation is usually required

Cyanosis

• Pulmonary/Cardiac/Haematological/Metabolic disorders
• Cyanosis without laboured breathing (“silent tachynpoea”) = Congenital cardiac disease
  • Usually right-to-left shunt (bypassing lungs) or a decrease in pulmonary blood flor
• Methaemoglobinaemia may mimic CHD
  • Discrepancy between arterial blood oxygenation and co-oximetry
• If irregular or shallow breathing, may indicate sepsis, meningitis, cerebral oedema or intracranial haemorrhage
• If laboured breathing, suggests pulmonary disease

Pneumonia

• Common bacterial
  • Group B strep, E. coli, Listeria, Hib, S. pneumoniae, Klebsiella, Enterobacter
  • Usually fulminant within 48 hours of life, likely acquired in utero
• Nosocomial in premature infants
  • S. aureus, Pseudomonas
• Chlamydia
  • 3-16% of exposed neonates
  • Usually after 3 weeks of age accompanied by conjunctivitis in 50%
  • Often afebrile, staccato cough
• Bordatella pertussis
  • Pneumonia + paroxysmal coughing/cyanosis/post-tussive emesis
  • Apnoea may be only symptom. Whoops do not occur in neonates
  • Suspect if adult caregiver has persistent cough

Congenital cardiac disease

• Tachynpoea without distress
• Well-developed neonate with unexplained cyanosis and tachynpoea is CHD until proven otherwise
• Duct-dependent lesions e.g. hypoplastic left heart syndrome, coarctation of aorta present with shock and acidosis upon duct closure in first week of life
• Left-to-right-shunting e.g. ASD, VSD tend to present later with CCF
• Prostaglandin E1 0.05-0.1mcg/kg/min titrated according to improvement in PaO2

Neuromuscular disease

• Shallow breathing and tachynpoea if weak
• Infantile botulism: Constipation, weak cry, feeding difficulties and tachypnoea
  • Ocular palsies, apnoea, weakness, hypotonia and lethargy are late signs
• Also consider, HIE, down syndrome, spinal cord lesions, myaesthenia gravis, metabolic disorders and myotonic dystrophy

Respiratory distress with abdominal signs

• Consider abdominal catastrophe such as necrotising enterocolitis, malrotation of midgut volvulus, congenital duplications or stenoses

Feeding difficulties

• Not fully established pattern until 1 month old
• If weight gain adequate and infant satisfied = adequate
• Consider upper GI/resp abnormalities if difficulties latching or swallowing e.g. stenosis, strictures, laryngeal clefts or cleft palate or double aortic arch compressing trachea/oesophagus

Vomiting

• Uncommon in first weeks of life (unlike regurgitation)
• If presenting at birth
  • Tracheo-oesophageal fistula (with oesophageal atresia)
  • Upper GI obstruction e.g. duodenal atresia (DS) or midgut malrotation
  • Raised ICP, metabolic disorders or sepsis must be considered
• Pyloric stenosis
  • Projectile vomiting after feeds classically 6 weeks to 6 months of age
  • Typically first-born males
  • Non-bilious or blood. Appears well between episodes
  • Left-to-right gastric waves/olive under liver edge
  • Classic hypochloraemic metabolic alkalosis uncommon now due to USS availability – Fix first

• Malrotation
  • Usually presents in first month with sudden bilious vomiting
  • 1/500 live births and 50% diagnosed in first month
• Volvulus
• Incarcerated hernias
  • Mostly 2 month to 1 year
• Intussusception
  • Mostly 2 month to 1 year
• Metabolic or endocrine
  • Always do glucose and gas if significant vomiting
  • Dextrose-containing fluid is usually adequate treatment in initial phase

Necrotising enterocolitis

• Premature (and rarely term neonates)
• Feeding intolerance, abdominal distension, bloody stools, discolouration of abdominal wall, apnoea and shock
• Pneumotosis intestinalis and hepatic portal gas on AXR
• Left lateral decubitus abdominal X-ray may show free gas if perforated
• Bowel rest, broad-spec antibiotics

Blood in the diaper

• Confirm actually blood e.g. orange urinary crystals not uncommon
  • Can test with FOBT
• Confirm GI vs. vaginal/urinary
  • Vaginal bloody discharge not uncommon in female neonates due to withdrawal of maternal oestrogen
• Examine anus
  • Fissure common but failure to see does not rule out diagnosis
• First 2-3 days of life, consider swallowed maternal blood
  • Can confirm with Kleihauer test of bloody sample

• Always consider NEC, coagulopathies, colitis and congenital defects
• Cow’s milk allergy
  • IgE-mediated disorder (but most just have intolerance)
  • Get altered bowel mucosa with gassy/bloody/mucousy stools, painful feeds and worsened reflux
  • Diagnosis confirmed by eosinophils in stool and resolution with avoidance of cow’s milk
• If single event and well, can observe as an outpatient

Diarrhoea and dehydration

• Infectious diarrhoea uncommon in neonates
• Small volumes of stool loss can cause considerable dehydration
• Serum electrolytes (esp. sodium and glucose) should be measured in any neonate with diarrhoea (though little value in older children)
• Stool and urine samples are useful
• Admit to hospital
• Trial oral rehydration if <5% dehydration
• Continue breastfeeding + ORS
• Always consider more serious cause in diarrhoea, particularly if bloody or mucous, including NEC, intussusception or volvulus

Abdominal distension

• May be normal due to lax musculature, large intra-abdominal organs and swallowed air
• If comfortable, soft abdomen and feeding well not an issue
• May also indicate bowel obstruction, NEC, ileus, volvulus, intussusception or solid organomegaly e.g. congenital issue or tumour

Constipation

• Infants may easily go 5-7 days without a bowel motion
• However, if never passed stool or failure to pass meconium within first 48 hours of life, consider intestinal stenosis, Hirschprung’s or meconium ileus associated with CF
• If starts in first months of life, consider Hirschprung’s, hypothyroidism, anal stenosis or anteriorly displaced anus
• Always examine lumbosacral spine for dysraphism
• Hypothyroidism
  • Constipation, feeding problems, weak/hoarse cry, large anterior fontanelle, hypothermia, hypotonia and peripheral oedema

Neonatal jaundice

• 60% of term babies and 80% of preterm suffer jaundice in first week of life
• 3.2% of babies require phototherapy
• Mild jaundice persisting up to 10 days can be physiological (or 3 weeks if pre-term)
• Early onset <24 hours is a risk factor for severe hyperbilirubinaemia requiring treatment
• Investigations into cause are warranted if:
  • Early onset <24 hours
  • Unwell child
  • Prolonged
  • Elevated conjugated bilirubin

Risk factors

• Maternal risk factors
  • Blood group O
  • Rhesus negative
  • Known red cell antibodies
  • Previously jaundiced baby
  • FHx of haemolytic disorders
  • East Asian/Mediterranean

• Neonatal risk factors
  • Breast milk
    • Beta-glucuronidase in breast milk increases breakdown of conjugated to unconjugated bilirubin in gut
    • Lipoprotein lipase and non-esterified fatty acids inhibit normal bilirubin metabolism
  • Delayed colonization of gut resulting in high concentration of bilirubin in gut
  • Dehydration if delayed milk letdown
  • Haemolytic disease
  • Polycythaemia
  • Haematoma
  • Bowel obstruction
  • Infection
  • Prematurity
  • Male

• Factors that increase level of free bilirubin and risk of kernicterus
  • Hypoalbuminaemia
  • Acidosis
  • Hypothermia
  • Infection
  • Certain medications
• Factors that have lower threshold for treatment
  • Haemolytic disease of the newborn
  • G6PD
  • Asphyxia
  • Lethargy

• Medications that cause bilirubin displacement off albumin
  • Digoxin
  • Diazepam
  • Salicylates
  • Frusemide
  • Hydrochlorothiazide
  • Ceftriaxone
  • Ibuprofen
  • Sulfamethoxazole (sulfur medications also interfere with bilirubin metabolism)

Differential

• Common causes of pathological jaundice
  • Haemolysis – Haematoma, ABO/Rh incompatibility
  • Decreased conjugation – Congenital hypothyroidism, Gilbert syndrome
  • Decreased excretion – Biliary atresia, CF
• Less common causes of pathological jaundice
  • Haemolysis – Enzymopathy (G6PD), Membranopathy (spherocytosis), haemoglobinopathy (thalassaemia)
  • Reduced conjugation – Crigler-Najjar, hypopituitarism
  • Liver cell damage – TORCH, IEM
  • Reduced excretion – Biliary atresia, bowel obstruction, pyloric stenosis, meconium ileus

• Physiological jaundice
  • Shortened red cell lifespan, decreased intestinal bacterial colonisation, decreased neonatal glucuronyl transferase function and relative polycythaemia all lead to increased enterohepatic circulation
  • Excessive levels can lead to permanent kernicterus
  • Usually arises day 2 and peaks at day 3 (term) to 5 (preterm)
  • Resolves by 10 days (term or 3 weeks (preterm)
  • Investigate if baby seems unwell or conjugated
  • All get SBR

• Breastfeeding jaundice (aka starvation jaundice)
  • Dehydrated due to exclusive breastfeeding with poor feeding
• Breast milk jaundice
  • Due to substances that inhibit glucuronyl transferase activity
  • May start at day 3-4 and peak at week 3
  • Unlikely to cause kernicterus and should keep breastfeeding

• Prolonged jaundice
  • Defined as >2 weeks in term and 3 weeks in preterm
  • More common in breastfed babies
  • Usually due to inadequate breastmilk nutrition or breast milk jaundice
  • Less common causes include:
    • Unconj: Infection, G6PD, spherocytosis, pyloric stenosis, Crigler-Najjar, Gilbert
    • Conj: Biliary atresia, Alagille syndrome, congenital hypopituitarism
    • Mixed: Hypothyroidism, IEM

Timing of onset

• <24 hours: 
  • Probably pathological and high risk of kernicterus
  • Haemolysis (ABO or Rh incompatability), congenital infection (TORCH), excessive bruising from birth, concealed haemorrhage, acquired infection
  • Haemolysis suggested by rapid rise in bili, anaemia, pallor, unconjugated bilirubinaemia, reticulocytosis, hepatosplenomegaly and positive family history
• 2-3 days
  • Usually physiological
  • Early-onset breastfeeding jaundice
  • Crigler-Najjar (familial non-haemolytic icterus syndrome with poor prognosis)

• 3d-1 week
  • Bacterial sepsis, UTI, TORCH
• >1 week:
  • Breast milk jaundice, acquired infection, biliary atresia, congenital and acquired hepatitis, red cell membrane defects (e.g. sickle cell, spherocytosis), red cell enzyme defects e.g. G6PD deficiency), haemolysis due to drugs, hypothyroidism, galactosaemia/fructosaemia, pyloric stenosis
• Persistent jaundice in first month of life
  • Hepatitis, cytomegalic inclusion disease, syphilis, toxoplasmosis, Crigler-Najjar, congenital biliary atresia and galactosaemia
  • Physiological jaundice can also be prolonged in the setting of hypothyroidism or pyloric stenosis

Clinical assessment

• Hx
  • Maternal infections during pregnancy/blood group and antibodies
  • Gestational age
  • Feeding patterns and type
  • Breastfeeding issues
  • Stool history including timing of first stool, colour and frequency
  • Urine output
  • Fever history
  • FHx of neonatal jaundice

• Stools and wet nappies
  • Pale stools/dark urine = Conjugated until proven otherwise
  • If unwell, need broad Ix
  • 4 or more wet nappies by 72 hours of age = adequate breastfeeding
  • 3 to 4 stools per day by 4^th day of life is normal

• Examination
  • Cephalocaudal direction of jaundice (Kramer’s rule) although not reliable
  • Cephalhaematoma
  • Fontanelle bulging/sunken
  • Palpate for hepatomegaly/splenomegaly

• Transcutaneous bilirubin
  • Screens only for unconjugated hyperbilirubinaemia
  • Suitable for gestational age >35 weeks and post-natal age >24 hours
  • Not recommended if:
    • Prolonged jaundice
    • Suspected conjugated hyperbilirubinaemia
    • Baby on phototherapy or had it
  • If >250micromol/L or within 50 of nomogram, measure total serum bilirubin

• Total serum bilirubin
  • Gold standard
  • If severe, prolonged or unwell baby  Need to measure total, conj and unconj
  • Measure if baby visibly jaundiced and:
    • <24 hours old
    • <35 weeks gestation
    • Unwell
    • Severely jaundiced
    • Prolonged jaundice
    • Previous phototherapy
    • Transcutaneous above or within 50micromol/L of threshold

• Signs of acute bilirubin encephalopathy
  • Lethargy
  • Poor feeding
  • Vomiting
  • High pitched cry
  • Hypotonia followed by hypertonia
  • Opisthotonus
  • Seizure
• Chronic bilirubin encephalopathy (kernicterus)
  • Evident in first year of life
  • Athetoid cerebral palsy, gaze paralysis, hearing loss
• BIND (Bilirubin-induced neurological dysfunction)
  • Subtle neurotoxic effects with hx of neonatal hyperbilirubinaemia
  • Muscle tone abnormalities, hyperexcitable neonatal reflexes, speech and language disorders, sensorineural hearing loss, visuomotor dysfunction

Risk factors for kernicterus

• Major risk factors for kernicterus
  • Predischarge bilirubin in high-risk zone
  • Jaundice in first 24 hours
  • Blood group incompatibility or haemolytic disease
  • Gestation <36 weeks
  • Previous sibling received phototherapy
  • Cephalhaematoma
  • Exclusive breastfeeding, esp. if poor feeding or excessive weight loss
  • East Asian race

• Minor risk factors
  • Predischarge bilirubin in intermediate-risk zone
  • Gestational age 37-38 weeks
  • Jaundice prior to discharge
  • Previous sibling with jaundice
  • Macrosomic infant to diabetic mother
  • Maternal age >25
  • Male gender

Investigations

• <24 hours
  • If well with no risk factors and jaundice is below treatment threshold:
    • FBC, TSB, ABO Group, Direct Coombs + Maternal group and antibody
  • If concerns re: hydration: UEC
  • If concerns re: infection: BC, CRP, Urine MCS, TORCH screen
  • If concerns re: IEM: Screen for galactosaemia, tyrosinaemia
  • If concerns re: liver disease: LFT

• >24 hours
  • Maternal Group and antibodies
  • Infant Group and antibodies + Direct Coombs
  • TSB
  • Other tests as indicated

• Prolonged jaundice
  • Serum bilirubin: Total, conj, unconj
  • FBC
  • TFT
  • LFT
  • Check newborn screening tests
  • Consider:
    • G6PD screen (esp. if male and FHx), glucuronyl transferase deficiency, hereditary spherocytosis/elliptocytosis
    • CF testing
    • IEM
    • Urine MCS, CMV and reducing substances (galactosaemia)
    • Abdominal USS

Treatment

• Rx as per nomogram
  • Phototherapy if unconjugated
  • Exchange transfusion if extreme
  • Risk factors for lower cut-offs include haemolysis risks, sepsis, asphyxia, hypoalbuminaemia and acidosis
  • Conjugated is a surgical emergency (e.g. biliary atresia)

Eye complaints

• Watery eyes
  • Clear discharge and crusting are common due to narrow nasolacrimal ducts
  • 6% of newborns have congenital nasolacrimal duct obstruction
  • Usually resolves spontaneously and only needs antibiotics if dacryocystitis or conjunctivitis ensues
• Red eyes
  • Consider abrasion
  • Acute glaucoma is rare but results in red, teary eye with cloudy cornea and raised IOP

• Eye discharge
  • 1.6-12% of neonates suffer conjunctivitis
  • Day 1: May be due to chemical irritation from antimicrobial prophylactic agents used in delivery room (occurs in first day of life usually)
  • Day 3-5: Gonococcal conjunctivitis peaks
  • After week 1 through to end of first month: Chlamydial conjunctivitis
  • Also consider HSV

• Chlamydial conjunctivitis
  • Mild to severe with thick mucopurulent discharge and pseudomembrane formation
  • May have concomitant pneumonia
  • Treat with oral erythromycin (80% effective)
  • Topical treatment not indicated
• HSV conjunctivitis
  • Vesicles anywhere on body with conjunctivitis suggests HSV and warrants full sepsis evaluation including LP for HSV and Rx with aciclovir

• Gonococcal conjunctivitis
  • Can be typical bacterial conjunctivitis
  • Hyperacute with profuse discharge at its most severe with oedema of both eyelids
  • Has ability to invade layers of eye causing corneal ulceration
  • Always perform gram-stain and culture + Chalmydial swabs for PCR for neonatal conjunctivitis
  • Treat with Cefotaxime (ceftriaxone displaces bilirubin in neonates)
  • Irrigate eyes with saline and at frequent intervals
  • Topical therapy otherwise not indicated

Neonatal varicella

• Most likely if mother gets varicella in 2 weeks prior to delivery
• Fever, vesicular rash +- invasive pneumonia/meningoencephalitis/hepatitis
• 25% mortality
• Mother should receive acyclovir to reduce complications in her but this DOES NOT reduce risk to fetus
• If delivery occurs within 5 days of onset of rash, neonate should receive VZIG

Congenital varicella syndrome

• Infants of mothers who had varicella between 8 and 20 weeks gestation
• Transmission risk is around 2% (low)
• Low birth weight, atypical scarring of skin, cataracts, cerebral cortical atrophy and global developmental delay
• No way to prevent or treat

TORCHES infections

• Toxoplasmosis
• Rubella
• CMV
• Herpes
• Syphilis
• Agents that cross the placenta and may be asymptomatic at birth through to multisystem involvement

• Clinical signs that raise suspicion (vs. acquired infection from delivery) include:
  • IUGR, microcephaly, hydrocephalus, intracranial calcifications, chorioretinitis, cataracts, myocarditis, pneumonia, hepatosplenomegaly, conjugated hyperbilirubinaemia, anaemia, thrombocytopaenia, hydrops fetalis and skin manifestations
  • Often cause an encephalitis with subsequent sensorineural hearing loss, seizures, blindness and neurodevelopmental concerns

Omphalitis

• Neonatal infection where umbilical stump is colonised from maternal birth tract bacteria
• May remain localised or spread to abdominal wall cellulitis, peritoneum, portal vessels or liver
• Can result in necrotising fasciitis

CSF in neonates

• May normally show elevated protein, glucose, leukocytes, PMNL’s
• Often xanthochromic due to elevated bilirubin and protein levels
• Normal opening pressure is 1-10cm in children, 6-20cm in children over 8 and up to 25cm in obese patients
• Intraventricular haemorrhage can result in:
  • Elevated CSF protein, leukocytes
  • Hypoglycorrhachia
• Low glucose also seen in:
  • Chemical meningitis
  • Inflammatory conditions
  • SAH
  • Hypoglycaemia
• There is no pathological process that causes raised CSF glucose levels other than raised serum glucose

Neonatal abstinence syndrome

• Manifestations usually within 48 hours
• Rarely symptoms can appear as late as 4-6 weeks
• Tremors and irritability are most common
• Other signs
  • Wakefulness, hyperacusis, hypertonicity, tachypnoea, diarrhoea, poor feeding, vomiting, high-pitched cry, fist  sucking, weight loss and fever

Last Updated on November 10, 2021 by Andrew Crofton