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