Neonatology Flashcards
what are the cardio changes that occur during transition from fetus to new-born?
3 shunts in utero - FO, DA, DV.
What is HIE?
Hypoxic Ischaemic Encephalopathy.
evidence of hypoxia/ ischaemia during labour + delivery + clinical evidence of encephalopathy
hypoxia evidence- CTG (cardiotocopgraphy), umbilical cord blood gas Indic acidosis, prolonged resus at birth.
encephalopathy evidence- tone, reflexes/breathing, loss of consciousness
when should a newborn pass its first poo? what is first poo called? What might you be concerned about if it is delayed?
within 48h
Meconium
CF/ Hirschprung’s Disease
what are the presenting features of Respiratory Distress Syndrome? What are the RF? And it’s pathophys?
RF: prematurity, maternal DM, meconium aspiration, severe resp infection, severe HIE
Presenting Features: Tachypnoea >60/min, signs respiratory distress e.g. chest wall recession (subcostal + sternal), nasal flaring, expiratory grunting to maintain PEEP, cyanosis if severe.
Inadequate surfactant (prod Type 2 pneumocytes) into alveoli to reduce surface tension which maintains Positive Expiratory Pressure and prevents alveolar collapse during expiration.
Pressure ∝ 1/r^4
Premies more at risk bc smaller alveoli ie smaller r therefore more P to open them and greater surface tension bc less surfactant being produced so higher chance of alveolar collapse.
What does RDS look like on CXR? How is RDS managed?
Bell shaped thorax, bilateral diffuse ground glass appearance due to
usually bilateral + symmetrical
bronchograms may be visible.
carefully controlled O2 therapy trying to maintain sats between above 91% (prevent NEC) but not above 95% (prevent ROP).
Exogenous surfactant either via tracheal tube/ catheter.
Non-invasive ventilation e.g. CPAP / high flow Nasal Cannula. Invasive if req via intubation but comes with risks to baby’s lungs.
List the common problems faced by premies?
respiratory distress syndrome, apnoea of prematurity, necrotising enterocolitis, infection, Poor Gylcaemic control, chronic lung disease, Retinopathy of Prematurity, Poor Gylcaemic control, poor temp control, intraventricular haemorrhage.
How does Necrotising Enterocolitis present? What are the RF for NEC?
RF: prematurity, low birth weight, hypoxia/ poor perfusion eg. baby has HIE, enteral fed but Breast Milk is protective, infection (cytokines interfere with gut mucosal perfusion)
Clinical signs: Abdo distension, discoloured abdomen, visible veins/ visible peristalsis, feed intolerance, increased volume of aspirate noted before feeding initiated may be green/ red due to bile/ blood, bloody stools. increased sepsis indicators - increased O2 req, more freq desaturations, high PCO2, high lactate, low Na+, metab acidosis.
What are the pathonomonic/ indicators of NEC on AXR?
- Pneumatosis Coli (earlier sign)- air within intestinal wall (intramural). see dilated bowel loops with stacking (in a row laterally)
- Fixed loop- no change in position of the bowel over hours when re XRd
- Football (American) sign (late sign)- perofrated viscus massive pneumoperitoneum best seen on lateral as black space above viscus. On AP see large shadow and can visualise the falciform ligament.
- Can also see air below liver/ surrounding portal vessels.
How is NEC managed?
Depends on stage (Bells)
Less severe stages (1 and 2)- stop oral feeds, NBM 10-14d, Broad spectrum Abx, parenteral nutrition. may req circulatory + ventilatory support.
If severe + perf req surgical excision
What is ROP? How does it present?
retinopathy of prematurity resulting from proliferation of new abnormal vessels that bleed, fibrose and detach the retina. Usually, blood vessels grow from optic disc outwards starting at 16w finishing 36w. If premature, the growth of vessels to all areas of the retina is incomplete causing the release of VEGF-1 and subsequent proliferation of abnormal vessels.
RF: <32w, <1.5kg BW, hyperoxaemia- O2 radicals, genetic susceptibility.
Detachment begins at outer retina and becomes more severe as moves towards the macula.
How is ROP managed?
Screening of at risk kids by Opthamologist, early intervention, Laser therapy.
COME BACK TO
what is an infection screen in newborn infants?
blood culture, LP, swabs if purulent eye discharge or umbilical infection, fbc + CRP, CXR if any signs of respiratory disease.
NO urine culture/ sample
what are the RF for neonatal infection?
prematurity, prelabour rupture of membranes, maternal UTI/ infection, chorioamnionitis, maternal GBS colonisation,confirmed/ suspected rupture membs >18h in preterm, invasive strep B in previous pregnancy baby, intrapartum fever >38,
What is IUGR? how is it different from SGA?
Intrauterine Growth Restriction: failure of growth in utero which may or may not result in SGA. IUGR is a failure to reach the full growth potential and is a risk factor for preterm delivery.
Small for Gestational Age: Birth weight <10th centile for gestational age.
- Symmetric SGA- all growth parameters symmetrically small suggestive of effect from early pregnancy e.g. small parents (constitutional) or genetic.
- Assymetric SGA- weight centile< length and head circumference usually bc IUGR due to late insult e.g. pre-eclampsia. (Ie headsparing)
What are the common causes of IUGR?
maternal substance misuse/ smoking, maternal HT, maternal malnutrition, maternal meds e.g. warfarin/ steroids/ anticonvulsants, TORCH, asthma, pre-eclampsia, sickle cell, SLE, antiphospholipid, diabetes associated vasculopathy, placental abruption, fetal genetic disorders, syndromes, metabolic disorders, congenital malformations e.g. CHD, diaphragmatic hernia, abdominal wall defects, congenital infections.
