Neonatal + newborn Flashcards
Causes (up to 2 weeks) of neonatal jaundice
<24 hrs after birth = sepsis (most common - TORCH infections or maternal vaginal tract organisms), ABO incompatibility + Rhesus disease (more likely if difficult birth due to blood mixing) 24 hrs - 2 weeks = physiological, breastmilk, dehydration, infection, haemolysis

Causes of prolonged jaundice
Unconjugated = physiological/ breastmilk, infection, hypothyroidism, haemolytic anaemia, high GI obstruction, G6PD Conjugated = bile duct obstruction, hepatitis Biliary atresia = surgery needed in 6 weeks >14 days in term, >21 days in pre-term infants
Complications of jaundice
Kernicterus = due to deposits of bilirubin in basal ganglia + brainstem S+S = lethargy, poor feeding, seizures, opisthotonus (hypertonia) RF: preterm, hypoxia, acidosis

What is physiological jaundice?
Bilirubin rises as infant is adapting, infant is slow to conjugate and excrete it Rise in unconjugated Not apparent for 24 hours. Fades by 14 days Common in preterms 2/3 normal babies get it Associated with difficulty establishing feeds - particularly new mums + breastfeeding
S+S jaundice
Starts at head/face and spreads Yellow discolouration of skin + sclera Dark urine + pale stools (if conjugated)
Investigations + management of jaundice + SE
<24hrs: FBC, blood group, DCT (Direct Coombs test), U+E, sepsis screen, bilirubin (conjugated/ unconjugated/ total) Over 24hrs: just bilirubin Phototherapy with light at wavelength 450 (from blue-green band). Check bilirubin every 6-8 hrs if severe, every 10hrs otherwise. Take off phototherapy when 50 below treatment line. Check bilirubin again after treatment, then discharge SE = temp instability, macular rash, bronze skin discolouration Exchange transfusion if severe

Causes of birth asphyxia
Failure of gas exchange across placenta due to: prolonged uterine contractions, placental abruption, ruptured uterus Interruption of blood flow due to cord compression, shoulder dystocia, cord prolapse Inadequate maternal placental perfusion due to IUGR, HTN

Hypoxic ischaemic encephalopathy
If evidence of severe hypoxia, resuscitation needed, evidence of hypoxic damage
S+S of birth asphyxia (mild, moderate, severe)
Mild = irritable, responds excessively to stimulation, hyperventilation Moderate = abnormalities of tone + movement, seizures, can’t feed Severe = no movements, hypo/hypertonia, prolonged seizures
Management of asphyxia
Respiratory support Fluid restriction Mild hypothermia

Types of pigmented birthmarks
Moles Cafe au lait spots Mongolian blue spots

Types of vascular birthmarks
Macular stains (salmon patches) Haemangiomas Port wine stains

CNS conditions causing skin lesions
Neurofibromatosis = cafe au lait spots Tuberous sclerosis = seizures, developmental delay, ash leaf-shaped macules on trunk, angiofibroma (papules over the nose), periventricular tubers (white spots at edge of ventricles on CT) Sturge Weber syndrome = unilateral port wine stains, intracranial haemangioma, presents with hemiplegia seizures, learning problems, glaucoma

Stork marks
Flat, pinkish capillary haemangiomas on forehead + eyelids. Fade over 2 years

Port wine stain
Capillary haemangioma (naevus flammeus) Starts pale then darkens

Strawberry mark
Soft, bright red capillary haemangioma Appears in days after birth, enlarges in first 6 months White areas develop Disappear before school age

Albinism in black vs white people
White = autosomal recessive Black = autosomal dominant

Mongolian blue spots
Large blue-grey patches, commonly over lumbosacral area + buttocks Common in asian + blacks Gradually fade
Cephalhaematoma causes
Bleeding below periosteum, confined within margins of skull sutures - doesn’t cross suture lines Common during assisted delivery

Subglial/ suba[pneurotic lesion S+S
Above periosteum Crosses suture line Life-threatening

Haemolytic disease cause
Increased red cell destruction Due to mother being negative for the antigen (anti-D, A, B or anti-Kell) Baby is positive Mother creates antibodies which cross placenta causing haemolytic anaemia (IgG crosses placenta)
Haemolytic disease in neonate S+S
Increased reticulocyte count Increased unconjugated bilirubin Jaundice Anaemia Hypoproteinaemia
Diagnosis of haemolytic disease
Positive direct anti-globulin test (Coomb’s)

Management of haemolytic disease
Transfusion + phototherapy
Complications of prematurity
Respiratory distress syndrome Hypoglycaemia/ calcaemia Jaundice Retinopathy Anaemia Necrotising enterocolitis Inguinal hernias Patent ductus arteriosus

Pathology of respiratory distress syndrome
Deficiency of surfactant Alveoli collapse = atelectasis Inadequate gas exchange Proteinaceous exudate seen on histology

S+S respiratory distress syndrome
CO2 retention = resp failure >60 breaths a min Chest wall recession Nasal flaring Expiratory grunting Cyanosis
X ray findings with RDS
Hazy, ground glass appearance

Management of RDS
Glucocorticoids given antenatally Surfactant therapy CPAP/ high flow

CPAP vs highflow
Continuous positive airway pressure Highflow = humidified air
IUGR causes (symmetrical vs asymmetrical)
Symmetrical = head circ equally reduced, due to prolonged IUGR, usually due to chromosomal abnormalities, congenital infection, maternal drug/ alcohol, chronic medical condition Asymmetrical = abdo circ is less than hea Usually due to placental dysfunction (pre-eclampsia, multiple pregnancy, maternal smoking)
Risks to fetus for IUGR
Intrauterine hypoxia Asphyxia during labour Hypothermia, hypoglycaemia, hypocalcaemia Polycythaemia
Talipes equinovarus - what is it, what causes it
Club foot Postural = caused by intrauterine compression Secondary to oligohydraminos, malformation or neuromuscular disorder Associated with DDH

S+S talipes equinovarus
Entire foot inverted + supinated Forefoot adducted Heel rotated inwards + in plantar flexion Affected foot is shorter Calf muscles thinner
Management of club foot
Plaster casting + bracing (Ponsetti method)
What is a neonate?
Term - up to 28 days Pre-term - up to 44 weeks gestation
Causes of conjugated jaundice?
Bile duct obstruction, hepatitis Biliary atresia = surgery needed in 6 weeks
What is the NICE treatment threshold graph for?
Jaundice Uses total bilirubin + age (in days) to show whether it needs treating with phototherapy or exchange transfusion Slope at beginning = lower threshold in first few days of life to stop acceleration

Conjugated jaundice - treatment + complications
Doesn’t cause kernicterus due to not crossing blood brain barrier Therefore doesn’t need to be treated with phototherapy Treat underlying cause
When will reflux resolve?
Usually by 10-18 months
Difference between reflux + GORD
GORD - negative symptoms
What are the types of spina bifida?
Myelomeningocele - most severe, spinal cord protruding with no skin covering Meningocele - meninges protrude out (spinal cord still covered) Occulta - vertebrae don’t form properly, causing small gap in spine.

What is possetting?
Blowing bubbles after feeding Feeds well + gains weight - no problem
What are the TORCH infections?
Toxoplasmosis Other (syphilis, VZV, parvovirus B19) Rubella Cytomegalovirus Herpes
What is parvovirus B19 + effects on neonate?
Also called slapped cheek or Fifth disease Can cause anaemia in fetus + miscarriage High risk from 4-20 weeks gestation Immunoglobulins are checked - if negative, risk of getting virus. Checked after 1 month for signs of virus. If infected, referred to specialist clinic Check for growth + anaemia Can treat with intrauterine blood transfusion if baby is anaemic

Describe toxoplasmosis in pregnancy + how it affects neonate, + treatment
Parasite found in meat, cat faeces + unpasteurised goat milk Symptoms like flu - blood test for ab to infection if worried Causes congenital toxoplasmosis - can cause miscarriage/ stillbirth Causes hydrocephalus, calcifications of brain or retinochoroiditis Most dangerous in 1st + 2nd trimester Abx - spiramycin - reduces risk of transmission
What are the effects of syphilis in pregnancy?
Can cause miscarriage, stillbirth, IUGR, fetal hydrops or congenital syphilis, Hutchinson teeth
Screening offered to all women Treat with penicillin during pregnancy

What is the Jarich-Herxheimer reaction?
Complex allergic response to antigens from dead organisms, causing fetal distress + uterine contractions Occurs in syphilis
Herpes in pregnancy
Can cause neonatal herpes, affecting skin/ eyes/ mouth, CNS or disseminated infection Risk greatest if new infection acquired within 6 weeks of delivery Treat with acyclovir for 5 days + daily suppressive aciclovir until delivery (if in 3rd trimester) CS if 1st episode herpes in 3rd trimester
VZV infection in pregnancy + effect on neonate
If uncertain of immunity, check immunoglobulins If not immune + had significant exposure, give VZIG (effective up to 10 days after contact) Complications: pneumonia, hepatitis, encephalitis FVS in fetus: skin scarring, eye defects, hypoplasia of limbs, neuro abnormalities - due to reactivation of herpes in utero Complicates from 3 weeks to 28 weeks gestation

Rubella in pregnancy
Notifiable disease Investigate If rubella confirmed + <20wks, risk of congenital rubella syndrome Human normal immunoglobulin given if termination unacceptable

Congenital rubella syndrome S+S
Deafness Eyes - retinopathy, cataracts, glaucoma Congenital heart disease
Cytomegalovirus in pregnancy
Most common cause of viral congenital infection Causes hearing loss + neurological disability Causes flu like symptoms in mum No treatment during pregnancy - antivirals given to neonates after birth
CMV at birth - S+S
Jaundice Petechial rash Hepatosplenomegaly Microcephaly SGA Majority asymptomatic - will go on to have hearing loss
Pathology of G6PD deficiency
G6PD = enzyme used in to keep NADPH levels accurate See Heinz bodies on blood film X linked Most people asymptomatic

Drugs that precipitate haemolytic crisis in G6PD pts
Nitrofurantoin + quinolones Sulfonamides Dapsone Aspirin Vit K Sulfonylureas
What is favism?
Acute haemolytic crisis due to broad beans eaten in G6PD
G6PD consequences for neonates
Neonatal jaundice + haemolysis risk (early jaundice) No treatment
What is exomphalos?
Failure of gut to return to abdo cavity
Causes defect in abdo wall, with peritoneal sac protruding
Associated with trisomy 18 (15%)
Also called omphalocele

What is gastroschisis?
Intestines protrude through abdo wall

What is caffeine used for in neonates?
To wean off ventilation
What are the RF for tetralogy of fallot?
Rubella or alcoholism during pregnancy, poor nutrition or mother >40 y/o
What are the classical signs + symptoms of NEC?
Non specific signs, bloody stools, abdo distension, bilious vomiting, apnoea
Erythema
Bradycardic, shock, resp distress
What do you see on AXR in NEC?
double line due to intramural + intraluminal gas
What is the management of NEC?
NBM (gut rest for 2 weeks), NGT + IVI (drainage), IV abx, TPN, O2, surgical review (most recover by conservative medical management)
RF for NEC
Prematurity + low birth weight
What is a protective factor for NEC?
Breast milk
What are the complications of NEC?
perforation, strictures, short bowel syndrome, fistulae, abscesses, recurrence
What does a football sign mean on AXR?
black around umbilicus = free air (perforation) – because x ray is taken lying flat so air floats to top
If a neonate is unwell, what initial investigations would you do?
Blood gas
Bloods - sepsis screen
CXR + AXR
When do you get the sucking reflex?
35 weeks
What are signs of a stress response?
High glucose + high platelets
What investigations would you run for ?pyloric stenosis?
Blood gas - metabolic alkalosis - low potassium + chloride
USS - long, narrow pyloric canal
RF for pyloric stenosis
Male first born
6-8 weeks old
Management of pyloric stenosis
NBM + fluids to correct acid base balance (takes around 24hrs to correct)
Pyloromyotomy - open = Ramstedt’s procedure or laparoscopic