Level 2 - Neonates Flashcards
Define HIE?
- Gas exchange is compromised resulting in cardiorespiratory depression
- Brain injury secondary to hypoxia
Mortality of HIE?
- Severe HIE has 30-40% mortality rate and 80% of survivors have learning impairments, particularly cerebral palsy
Aetiology of HIE? (4)
o Failure of gas exchange across placenta (excessive or prolonged contractions)
o Interruption of umbilical blood flow (cord compression, prolapse)
o Inadequate maternal perfusion
o Inadequate postnatal cardiopulmonary circulation
Symptoms of mild, moderate and severe HIE? General features?
Mild HIE
- Irritable, excessive response to stimulation, hyperventilation, impaired feeding
Moderate HIE
- Abnormal tone, movement, cannot feed and seizures
Severe HIE
- No normal spontaneous movements or response to pain, abnormal tone, prolonged seizure, multi-organ failure
Cyanosis, low heart rate, acidosis
Describe the signs in HIE?
Abnormal neurological signs and seizures Persistent pulmonary hypertension Hypotension DIC Renal Failure Low glucose, Ca, Na
Investigations in HIE?
Blood gas - Acidosis aEEG - Used to confirm encephalopathy or identify seizures CT/MRI
Management of HIE?
Resuscitation - Baby will have respiratory depression Hypothermia Anticonvulsants Fluid Restriction Treat electrolyte imbalances - Low glucose, calcium, sodium
Define birthmarks?
- Birthmarks are coloured marks that are visible on the skin. They’re often present at birth or develop soon afterwards
Two types of birthmarks?
o vascular birthmarks (often red, purple or pink) caused by abnormal blood vessels in or under the skin
o pigmented birthmarks (usually brown) caused by clusters of pigment cells
Name the common vascular birthmarks?
Salmon patches
Infantile haemangioma
Port-Wine stain
Name common pigmented birth marks?
Cafe-au-lait spots
Mongolian spot
Congenital melanocytic nevus
What is Salmon patch? How common? What happens to them?
o Flat red or pink patches that can appear on a baby’s eyelids, neck or forehead at birth
o They’re the most common type of vascular birthmark and occur in around half of all babies
o Most salmon patches will fade completely within a few months, but if they occur on the forehead they may take years
o Often more noticeable when a baby cries because they fill with blood and become darker
What is an infantile haemangioma? How common and who do they tend to affect? Any treatment?
o Red to purple papules or plaques with a normal epithelial surface
o Compression leads to partial emptying and the colour becomes less prominent
o Haemangiomas are common, particularly in girls, and affect around 5% of babies soon after birth
o If they get bigger rapidly, or those that interfere with vision or feeding may need treatment
What are Port-wine stains?
o Deep pink or red patch present at birth and grows as the child grows
o May darken to purple, is flat; the overlying skin is normal. Later in life more papular lesions can occur within the patch
o Present for life and has no tendency toward involution
o Usually unilateral with a clear demarcation at the midline
Investigations in Port wine stain?
o If Sturge-Weber syndrome is suspected, MRI scan of the brain is required
o Optical coherence tomography
o Regular ophthalmic checks to exclude glaucoma should be carried out in the first three years of life
Management of Port wine stains?
o Refer as young as possible, usually around 1 year old, to a centre which has the laser and anaesthetic facilities
o Tunable pulsed dye laser (PDL)
o Surgical excision with or without cosmetic reconstruction may be required for lesions resistant to laser therapy
What are Cafe-au-lait spots? When should you see your GP? What could it be linked with?
o Caused by an increase in melanin content, often with the presence of giant melanosomes
o Coffee-coloured skin patches
o Common but if >six have developed by the time the child is five, you should see your GP
o Could be due to neurofibromatosis 1
What are mongolian spots?
o Caused by melanin within the deep layer of the skin (dermis)
o A benign, flat, congenital birthmark, with wavy borders and an irregular shape
o More commonly seen in darker-skinned people and usually covers the lumbosacral, buttocks, sides and shoulders
Colour and prognosis of Mongolian spot? What must happen?
o Normally disappears three to five years after birth and almost always by puberty
o Colour is blue, although they can be blue-grey, blue-black or deep brown
o They’re completely harmless and don’t need treatment
o May sometimes be mistaken for a bruise so NEED to be documented in notes if found
What are congenital melanocytic nevus?
o Initially appear as flat, pigmented lesions
o As the lesion ages, it tends to become raised and may become hairy
o Located in the area of the head and neck 15% of the time
Management of melanocytic nevus?
o Need to be aware of ABCD changes in malignant melanoma
o Typical small/medium lesions with no suspicious features usually require no investigation
o Dermoscopy and biopsy of suspicious lesions
o No treatment usually but can have done if suspicious
What is Sturge-Weber syndrome?
Neurocutaneous disorder classically presenting with:
Facial port wine stain affecting facial skin
Vascular abnormalities
Ipsilateral occipital leptomeningeal angioma
Venous hypertension
What complications of Sturge-Weber syndrome?
Develop progressive problems including glaucoma, seizures, stroke, and intellectual disability
How is diagnosis of SWS made?
Diagnosis of SWS is made if the cutaneous port-wine stain is associated with either brain or eye involvement (USS then MRI/CT needed)
Management of SWS?
Cosmetic camouflage creams can be used to help to conceal the port-wine stain
Carbamazepine
Pulsed dye laser (PDL) treatment is used for port-wine stain
General management of birthmarks?
Most haemangiomata require no treatment unless the patient is concerned about their appearance
Port-wine stains are usually treated by camouflage but the patient may wish to be referred for laser therapy
Definiton of cephalohaematoma?
- Subperiosteal swelling on foetal head and its boundaries
- Spread is restricted by suture lines that are adherent, so it is limited to the surface of one cranial bone
Where is cephalohaematoma most common?
- Commonest over parietal bones
Risk factors of cephalohaematoma?
o Malposition o Large infant o Instrumental delivery (forceps/Ventouse) Ventouse more likely to cause injury o Breech delivery o Prematurity o Primagravida
Symptoms and signs of cephalohaematoma?
- Centre feels soft
- Blood loss can cause anaemia and even hypotension
- Could have jaundice following blood breakdown
DDx of cephalohaematoma?
Caput succedaneum (extends beyond bone margins) Chignon (following forceps delivery)
Investigations of cephalohaematoma?
- Underlying skull fracture may be present. If suspected and thought to be depressed, CT or MRI scanning is required and surgery may be indicated
Management of cephalohaematoma?
- Usually resolves over several weeks
- Rarely this may require surgical removal for cosmetic reasons
- Jaundice needs treatment
Types of haemolytic disease in neonate?
Rhesus haemolytic disorder ABO incompatibility G6PD deficiency Spherocytosis Sickle Cell Disease Thalassaemia
What is Rhesus haemolytic disorder?
- Usually identified antenatally
- Presents with anaemia, hydrops, hepatosplenomegaly with rapidly developing jaundice
- Usually anti-D
- Antibodies may develop to rhesus antigens other than D and to the Kell and Duffy blood groups
What is ABO incompatibility?
- Now more common than Rhesus incompatibility
- Most ABO antibodies are IgM and do not cross placenta, but some blood group O women have IgG anti-A-haemolysin which haemolyses red blood cells of a group A infant
- Occasionally group B infants affected by anti-B haemolysins
Features of ABO incompatibility?
- Can cause jaundice – peaks 12-72 hours
- Anaemia is less severe and no hepatosplenomegaly
- Coombs test positive
What is G6PD deficiency?
- Mainly from Mediterranean, Middle-East and Far East
- Males mostly, develop severe jaundice
- Drugs need to be avoided
What is spherocytosis? Features? Diagnosis? Treatment?
- Autosomal dominant inheritance with FHx in 75%
- Early, severe jaundice in newborn infants
- May cause anaemia, jaundice, splenomegaly, aplastic crisis and gallstones
- Diagnosed on blood film
- Treatment with folic acid, splenectomy if symptomatic
Diagnostic clues towards haemolytic disease?
Increased reticulocyte count
Increased unconjugated bilirubin
Definition of prematurity?
- Infants born <37 weeks gestation
Epidemiology of prematurity?
- Leading cause of perinatal mortality
- 50% of perinatal deaths
- Prevalence 6% in singletons, 46% of twins, 79% of triplets
Risk factors for premature birth?
- History of preterm births
- Multiple pregnancy
- Cervical surgery
- Uterine anomalies
- Pre-existing medical conditions
- Pre-eclampsia
- IUGR
Symptoms of very preterm infant?
- Low birthweight
- Very skin thin
- Dark red colour
- No palpable breast tissue
- Males
o Scrotum smooth, no testes in scrotum - Females
o Prominent clitoris, labia minora protruding
Associated features of a preterm infant?
- Apnoeas common
- No coordinated sucking and often need TPN
- Jerky movements, startled easily
Investigations of premature baby?
- Monitor observations (HR, BP, RR, SpO2, To), weight, etc
- FBC (Haemoglobin, neutrophils, platelets), CRP, U&Es, lactate, glucose
- Blood cultures
- Mid-stream urine
- Speculum to rule out PROM
Management to delay delivery in preterm labour?
- Tocolytics could be used to delay and allow corticosteroids to work
Management of preterm infant?
- Transfer to NICU
o Early contact with mother
o Handling kept to a minimum as painful and affect oxygenation
o Airway/Breathing
Oxygen, High-flow humidified oxygen, CPAP
Mechanical Ventilation
o Keep warm
Heat lamp, wrapped in plastic wrap
o Arterial line for IV access
Circulatory support via transfusion, saline, inotropic drugs
o CXR all NICU infants for respiratory distress
o IV Antibiotics
Prognosis of preterm briths?
- Prognosis good after 32 weeks gestation
o Increased risk in Cerebral palsy
Define respiratory distress syndrome? Pathology? (RDS)
- Inadequate surfactant production causes air sacs to collapse on expiration and greatly increases the energy required for breathing
- Most alveolar surfactant produced >30 weeks
- Interstitial oedema makes the lung even less compliant which leads to hypoxia and retention of carbon dioxide
Epidemiology of RDS?
- Incidence and severity inversely proportional to gestational age
- Affects ½ of infants born at 28-32 weeks
Pathology of RDS?
- Caused by the inadequate production of surfactant in the lungs. Surfactant is normally produced by type II pneumocytes and has the property of lowering surface tension
Risk Factors of RDS?
o Premature delivery o Males o C-Section o Hypothermia o Maternal Diabetes
Secondary surfactant deficiency caused by what?
o Pulmonary infection, haemorrhage
o Meconium aspiration
Symptoms and signs of RDS?
- At delivery or within 4 hours: o Preterm delivery o Tachypnoea (>60/min), expiratory grunting, subcostal and intercostal retractions, diminished breath sounds, cyanosis and nasal flaring o Progress to apnoea, fatigue and hypoxia rapidly o Decreased cardiac output, hypotension, acidosis and renal failure
DDx of RDS?
- Pneumothorax, pneumomediastinum
- Infection (group-B strep), aspiration
- Transient tachypnoea of newborn
o Due to excess lung fluid - Congenital lung/heart defects
Investigations in RDS?
- Blood gases o Respiratory and metabolic acidosis - Pulse oximetry o Aim for 91-95% - Chest X-ray o Diffuse ground glass appearance o Air bronchograms - Monitor FBC, electrolytes, glucose, renal and liver function - Echo and cultures
Prevention of RDS?
o Dexamethasone offered to at risk women of preterm delivery from 23-25 weeks
Management of RDS?
o Delay clamping of cord to promote placental-fetal transfusion
o Wrap up baby warmly and take to NICU
o Oxygen
Via oxygen-air blender and can use CPAP
Mechanical ventilation if needed
o Surfactant replacement
Via endotracheal tube
Inositol is essential nutrient promoting surfactant maturation
o Fluids
10% glucose IVI if needed
o Antibiotics
Start antibiotics in all infants who present with respiratory distress at birth, after obtaining blood cultures
Complications of RDS?
o Alveolar rupture, intracranial haemorrhage, PDA, pulmonary hypertension
o Chronic lung disease, retinopathy of prematurity, neurological impairment if severe hypoxia
Define IUGR?
- Where a baby’s growth slows or ceases when it is in the uterus
- Part of wider group of SGA foetuses and often used synonymously
- Clinical definition and applies to neonates born with clinical features of malnutrition and in-utero growth restriction, irrespective of their birth weight percentile
Definition of SGA?
Estimated fetal weight <10th centile for age or head circumference <10th centile
Pathology of IUGR?
- Any mismatch between the supply of nutrient by the placenta and the demand of the fetus also leads to IUGR
Where is incidence highest in IUGR?
6x more common in developing countries
Risk factors for IUGR?
o Maternal age (<16, >35) o Twins o Placental dysfunction/abruption o Chronic hypertension/pre-eclampsia o Diabetes o Previous SGA baby o Previous stillbirth Smoker o Cocaine use
Classification of IUGR?
- Symmetrical
o Earlier in pregnancy
o All antenatal and postnatal measurements are reduced proportionally - Asymmetrical
o Later in pregnancy
o Antenatal scans all normal but reduced postnatal measurements - Mixed
Investigations in IUGR?
- At booking, every woman should have growth chart considering maternal age, parity, BMI, ethnicity and birthweights of previous children
- USS if:
o SFH measurement <10th centile or static growth - Serial measurements of amniotic fluid volume, foetal movements, foetal tone, foetal breathing and heart activity
- Umbilical artery doppler scan
Management of IUGR?
- If normal doppler aim for IOL at 37 weeks
- If abnormal then may need LSCS earlier
- Corticosteroids
o Foetal lung maturation - Keep warm and feed early as prone to hypoglycaemia
Complications of IUGR?
o Perinatal asphyxiation, meconium aspiration, persistent pulmonary hypertension, jaundice, NEC
o Poor growth and neurodevelopmental problems
o Obesity, metabolic syndrome, type 2 diabetes, CVD
Definition of congenital talipes equinovarus?
- Congenital talipes equinovarus is characterised by a permanent alteration of the morphology of the foot
- The foot cannot be placed flat on the ground when in the physiological standing position
Two types of talipes?
Positional
Congenital
What is positional talipes? How common? Management?
Normal foot that has been held in a deformed position in the uterus
Postural talipes is correctable with gentle passive dorsiflexion of the foot
This positional variant occurs about five times more often than congenital talipes equinovarus
Passive exercises by physio can help
What is congenital talipes? Types?
A fixed condition, which may be idiopathic or teratological
The idiopathic type is usually an isolated skeletal anomaly. It is usually bilateral, and has a higher response rate to conservative treatment
Teratological associated with genetic syndromes, neurological disorders and myopathies
Epidemiology of talipes?
- 50% are bilateral
- Males 2x more common
Aetiologies of talipes?
o Neuromuscular and anatomical causes (muscle fibre abnormalities, titling and rotation of the talus, hypoplasia of the anterior tibial artery)
o Polygenic multifactorial genetics
o Arrested fetal development
What may lead to positional talipes?
- Oligohydramnios, uterine anomalies and multiple pregnancy may lead to positional talipes due to fetal restriction
Associated conditions with talipes?
- Associations with spina bifida, cerebral palsy and arthrogryposis
Symptoms of talipes?
- Foot
o Inverted
o Adduction of forefoot relative to hindfoot
o Equinus (plantarflexion) deformity
o Sole of foot points medially - Heel is high and calf muscle is smaller
- Affected foot is smaller
Feature of congenital talipes?
- Foot is fixed and cannot be corrected completely
DDx of talipes?
Child with a limp
Investigations of talipes?
- Diagnosis made on clinical assessment
- Classed using Pirani scoring system
- Imaging helps class severity
o Xray AP and lateral standing
o USS
What is Ponseti method in managing talipes?
o Used in children up to 2 years old
o Stretching – the foot is re-positioned, and a cast is applied
o Re-cast weekly for several months
o Towards the end, Achilles tenotomy usually performed to lengthen the tendon
Botulinum toxin is sometimes used as an alternative to tenotomy
o The child wears special shoes or braces full-time for three months, then nightly for three years
What is the French functional method in managing talipes?
o Done in young children by specialist physios, foot gradually stretched and held in correct place with tape
Surgery in talipes?
o Not recommended as primary treatment
o Used when unbalanced growth
o Selective medial release, posteromedial release and cuboid subtraction osteotomy
