Neonatology Flashcards
Define ‘Pre-term’
Delivery before 37 weeks completed gestation
Extreme - before 28 weeks, Very Preterm - 28 to 32 weeks, Moderate - 32 to 37 weeks
Describe the aetiologies of Preterm Infants
25% planned (life threatening pre-eclampsia etc)
30% are due to PPROM
25% are due to emergency (severe infection, placental abruption)
State Naegele’s rule of EDD
LMP + 7d -3m +1y
If an EDD wasn’t noted, the age of the baby can be estimated using Dubowitz Scoring. What is it?
Uses external physical and neurological features to give a score which then gives a two week window of estimation
Neuromuscular - posture, popliteal angle, heel to ear
Physical - skin, lanugo hair,genitals, eye/ear
After birth the preterm will have a full range of bloods. Describe three other investigations required.
CXR (likely to require intubation so looks for any abnormalities which may complicate endotracheal tube)
AXR (check that central line via umbilical artery is in correct place, looks for NE)
Cranial USS (assess for intraventricular haemorrhage or white matter damage)
If a preterm birth is inevitable, what can be done antenatally?
Arrange delivery in tertiary centre delivery suite
Antenatal steroids
Magnesium Sulphate (neuroprotective)
At what age are preterm babies rescucitated?
<23 weeks ~ not performed
23-23+6 weeks ~ may be a decision not to
24-24+6 weeks ~ commenced unless severely compromised
> 25 weeks ~rescucitation and NICU
Name three things that can aid a newborns thermal regulation after delivery
Plastic Wrap
Heated Mattress
Overhead Lamp
What is the long term respiratory management considerations in preterm infants?
Surfactant Administration
Intubation and Oxygenation
Caffeine
What is the long term Cardiovascular management considerations in preterm infants?
Inotropes
Fluids
Ibuprofen/Indomethacin
What is the long term GI management considerations in preterm infants?
TPN
NG
Abx
Survival of preterm babies is rare before 23 weeks. Name four later complications in childhood of prematurity
Gross Motor Delay
Fine Motor Impairment
Behavioural Abnormalities
Speech and Language Abnormalities
Name a family support group for premature infants
Bliss
What are the five categories of withdrawing Paediatric care?
- The Brain Dead Child
- The Permanent Vegetative State
- No Chance (treatment delays death but doesn’t improve life quality or potential, not in best interest of patient)
- No Purpose (may be able to survive with treatment but it would not be in patients best interest , may leave them in a worse condition)
- Unbearable Situation (When child or family feel that more treatment is too much to handle)
Jaundice occurs in 60% of term infants and 80% preterm. What is the relevance of conjugation?
Unconjugated can be physiological or pathological
Conjugated is always pathological
Physiological jaundice starts at day 2-3 and is resolved by day 10. Give two causes.
Increased RBC break down (high concentration required in utero that is no longer needed)
Immature liver (lags behind and unable to conjugate at these high concentrations)
When can Physiological Jaundice become Pathological?
If baby is premature
If further extensive breakdown (eg from bruising)
Define Pathological Jaundice
A jaundice which requires treatment or further investigation
All jaundice within 24h is pathological
Give three risk factors for pathological jaundice
Prematurity
Low Birth Weight
Diabetic Mother
Describe the non physiological jaundice in terms of onset time frame - less than 24 hours
Haemolytic Disorders (Rhesus, ABO incompatibility, G6PD, Spherocytosis)
Congenital Infection
Describe the non physiological jaundice in terms of onset time frame - 24 hours to 2 weeks
Breast Milk Jaundice
Dehydration
Infection (UTI)
Haemolytic
Bruising
Crigler Najjar Syndrome
Describe the non physiological jaundice in terms of onset time frame - more than 2 weeks
Unconjugated: Infection, Hypothyroidism, Haemolytic Anaemia, High GI Obstruction
Conjugated: Bile Duct Obstruction, Neonatal Hepatitis
Describe four possible clinical features of Neonatal Jaundice
-Discolouration (examine sclera, gums, skin blanche)
-Drowsy (difficult to rouse, short feeds)
-Altered Muscle Tone
-Seizures
Bilirubin needs to be measured if the Jaundice is not visible to the naked eye. Describe the two methods.
Transcutaneous Bilirubinometer (if >35 weeks gestation and >24 hours old, can be used for repeats as long as level is under 250 and no treatment required)
Serum Bilirubin if <35 weeks, <24 hours old or previous level >250
Want to know total and conjugated/unconjugated
Name five further investigations for Neonatal Jaundice
Blood Group
Direct Coombs
FBC (haemoglobin and haematocrit)
Infection Screen
LFTs
Phototherapy is a management option for Neonatal Jaundice, how is this decided?
Treatment threshold graphs that are gestation specific
If above line - phototherapy initiated and bilirubin monitored
If below line by more that 50, and clinically well don’t repeat
If below line by less than 50 and well, repeat in 18-24 hours
How does Phototherapy work for jaundice?
Via Photo- Oxidation
Adds oxygen to bilirubin so it dissolves more easily
When should phototherapy be stopped?
6-12 hourly repeats once stable
Stop once more than 50 below threshold
Check for rebound 12-18 hours after stopping
Another option for Jaundice management is Exchange Transfusion. When is this used?
If Acute encephalopathy or very high levels (as per graph)
What can you give as an adjunct to pathological jaundice due to ABO/Rhesus incompatibility?
IVIG
Kernicterus is the main complication of Neonatal Jaundice, what is it?
Bilirubin induced brain dysfunction
Accumulates in CNS grey matter causing irreversible damage
Define Early Onset Neonatal Sepsis
Sepsis within the first 48 - 72 hours of life, most commonly due to GBS
State three methods of spread causing Neonatal Sepsis
Chorioamnionitis
Birth Canal
Haematogenous
Give two early and two late manifestations of neonatal GBS
Early - RDS, Pneumonia
Late - Sepsis, Meningitis
State five red flags of Neonatal Sepsis
-RDS starting more than 4hrs after birth
-Seizures
-Signs of Shock
- Abx given to mother around birth
- Suspected in another baby if multiple pregnancy
Give three differentials for Neonatal Sepsis
TTN
RDS
Meconium Aspiration
Describe the management of Neonatal Sepsis
Initial empirical IV Benzylpenicillin and Gentamicin
If meningitis suspected - Amoxicillin and Cefotaxime
Known GBS - Benzylpenicillin
Continued for 7-10d if positive blood culture, or 14 days if CSF culture positive
How would you manage raised CRP in first 24 hours of life but negative cultures?
5 days IV Antibiotics
Define Sudden Infant Death Syndrome
Sudden and unexplained death of a child under one (remaining unexplained even after post mortem and history review)
Describe the 1994 triple risk model of SIDS
Underlying vulnerability (eg premature)
Critical Development (1-3 months)
Exogenous Stressor (Sleeping Prone)
Give four risk factors for SIDS
-Smoking (maternal in pregnancy and passive)
-Alcohol and Substance Abuse
- Preterm Birth (often placed prone to improve resp function so should get used to sleeping on back pre discharge)
- Bed Sharing
Give three protective factors for SIDS
Breast Feeding
Dummies
Room Sharing
What is a Life Threatening Event Syndrome?
Combination of apnoea/change in colour/change in muscle tone/coughing/gagging
50% underlying condition 50% unknown
Describe a social benefit, and retraction to breast feeding
Benefit : It’s free
Detractions: Public Taboo
Give two medical benefits of breast feeding for the mother and the child
Child : Increased Immunity, Decreased SIDS risk
Mother: Decreased Breast Cancer, Decreased Ovarian Cancer
Why are feeding difficulties more common in preterm babies?
Coordination between suckling/swallowing and breathing is normally developed between 34-36 weeks
Give three broad causes for difficulty feeding in term babies
Anatomical Malformations (Cleft Palate, Tongue Tie)
Sleepiness (Hyperbilirubinaemia, Hypoglycaemia, Hypothyroidism)
Neurological (Strokes, Seizures, SAH)
Give four causes for feeding difficulties in infants
Cows Milk Protein Allergy
GORD
Colic
Lactose Intolerance
What is Colic?
Thought to be a combination of GORD, CMPA and Constipation
Crying more than three hours a day, more than three days a week for more than three weeks.
Drawing up knees and arching back
Give three points of the approach to a Dysmorphic Child
-Make an accurate diagnosis
-Recognise associated abnormalities and medical problems
- Optimise QoL
Describe the three types of dysmorphia in a child
Normal Spectrum of human variance (no medical significance)
Minor Anomaly (eg flat philtrum, bifid uvula)
Major Anomaly (has medical/surgical/cosmetic significance)
When should you suspect a genetic condition in a child?
Multiple minor anomalies (>3)
Or
More than one major anomaly
Or
One major and a few minor anomalies
Give an example of sex limited and sex influences expression
Limited - Hereditary Prostate Cancer
Influenced - Hypospadias
Define Malformation
Defect of morphogenesis in organ or structure
Can be isolated or part of a chromosomal disorder
Define Deformation
Abnormal form/position caused by extrinsic disruptive forces on developing foetus
Define Disruption
Destructive breakdown or interference with a normally developing structure
Define Dysplasia
Error of morphogenesis due to abnormal cellular organisation in a specific tissue (eg Achondroplasia)
Define Downs Syndrome
Genetic disorder caused by Trisomy 21 (non disjunction in maternal oogenesis, or mosaic)
Give 6 features of Downs Syndrome
Generalised Hypotonia
Low Set Ears
Upslanting Eyes
Flat Occiput
Single Palmar Crease
Intellectual Impairment (IQ 26-70)
Give four other pathologies associated with Downs
Congenital Heart Defects
Deafness
Cataracts
Leukaemia
How is Downs Syndrome diagnosed prenatally?
11-14wks - Combined Test (Nuchal Thickness, PAPP- A, bHCG)
15-20wks - Quadruple Test (AFP, Unconjugated Oestriol, bHCG, Inhibin A)
If deemed high risk (>1 in 150 chance) - NIPT (or amniocentesis)
How is Downs Syndrome diagnosed Post Natally?
Chromosome analysis via microarray showing Trisomy 21
Give four management points of Downs Syndrome
Specialist referrals (audiology, cardiology)
Genetic Counselling
Use of Downs Syndrome Association
Annual TFTs
What is the prognosis of Downs Syndrome?
Life expectancy well into adult life although most develop Alzheimer’s by 40 years old
Majority can live semi independent with supervision
What is Patau Syndrome?
Trisomy 13
Median survival of 8.5 days
Give 5 features of Patau Syndrome
SGA
Microcephaly
Cleft Lip
CHD
Polydactyly
What is Edwards Syndrome?
Trisomy 18
Median life expectancy is 74 days
Give 5 features of Edwards Syndrome
SGA
CHD (particularly VSD)
Short Sternum
Overriding fingers
Rocker Bottom Feet
What is Turners Syndrome?
Genetic disorder caused by non disjunction characterised by the karyotype 45,X
Give 5 features of Turners Syndrome
Short Stature
Neck webbing
Ptosis
Wide spread nipples
Puffy hands and feet
Give three associated anomalies of Turners Syndrome
CHD
Renal Abnormalities
Hypoplastic Ovaries
What is Digeorge Syndrome?
Genetic disorder caused by micro deletion on Chromosome 22
Characterised by ToF, Wide Nasal Bridge, Hypocalcaemia (Parathyroid Hypoplasia), T Cell Deficiency (Thymus Aplasia)
I.E CATCH 22
What is Marfans Syndrome?
Autosomal dominant mutation on fibrillin gene
Characterised by tall and slim, pectus malformation, scoliosis, high arched palate, lens dislocation and cardiac abnormalities
What is Noonan’s Syndrome?
Mutation on chromosome 12
Characterised by Pulmonary Stenosis, Short Stature, Broad Neck, Developmental delay
(‘Male Turners’)
What is Williams Syndrome?
Micro deletion on chromosome 7
Characterised by periorbital fullness, full cheeks, small spaced teeth, over friendliness
State four features of Angelman Syndrome?
Severe Developmental delay
Speech impairment
Ataxic Gait
Hand flapping
State the features of Fragile X Syndrome
Gaze Avoidance
Stereotyped Repetitive Behaviour
Resistance to change of routines
Commonest inherited cause of mental retardation
Describe four features of Prader Willi Syndrome
Floppy babies with feeding difficulties
Rapid Weight Gain between 1 and 6 years
Learning difficulties
Food foraging and behavioural problems
Define Hypoxic Ischaemic Encephalopathy
During perinatal asphyxia, gas exchange (placental or pulmonary) ceases resulting in cardio respiratory depression. Compromised cardiac output reduces cerebral perfusion.
Give 5 broad aetiologies of HIE
-Failure of gas exchange across placenta (placental Abruption)
- Interruption of Umbilical Blood Flow (cord compression)
-Inadequate maternal placental perfusion (hypotension)
- Compromised foetus (IUGR)
- Failure of Cardioresp abnormalities
How does HIE present?
Encephalopathy + Respiratory Failure + Myocardial Dysfunction + Metabolic Dysfunction + Other Organ Dysfunction
Describe mild HIE
Irritable, Staring eyes, Hyperventilation, Impaired Feeding
Describe moderate HIE
Marked abnormalities of tone and movement, cannot feed, may have seizures
Describe Severe HIE
No spontaneous movement, no response to pain, fluctuating tone, prolonged seizures
Describe some management considerations for HIE
-Respiratory support
-Treating clinical seizures with anticonvulsants
-Fluid restrict due to transient renal impairment?
Therapeutic Cooling - with blanket for 72h, aiming for 34 degrees (reduces metbaolic demand decreasing the impact of ischaemia
What is the prognosis of HIE?
If mild then complete recovery
If moderate and appear neurologically normal at two weeks - good
If severe - over 80% have neurodevelopmental disability
What is Respiratory Distress Syndrome?
Deficiency of surfactant to lower surface tension leading to collapse of alveoli
Common in infants born prior to 28 weeks, or infants of diabetic mothers
Give four clinical features of RDS (at delivery or within four hours)
-Tachypnoea
-Laboured breathing with chest wall recession
-Expiratory grunting
-Cyanosis if severe
What would be seen on a CXR of RDS?
Bilateral and diffuse ground glass appearance (generalised atelectasis)
Air bronchograms
Reduced lung volume
The level of respiratory support to manage RDS depends on severity of disease. Describe the options.
Nasal CPAP/High Flow Oxygen
Endotracheal Intubation and Surfactant (eg Curosurf - first dose as bolus)
Other than ventilators support, what managements should be considered in RDS?
Antibiotics (Penicillin and Gentamicin until Congenital Pneumonia is ruled out)
IV fluids until baby is stable
Gastric feeds with minimal volume
If preterm delivery is inevitable - maternal corticosteroids
What is Necrotising Enterocolitis?
Life threatening inflammation of the bowel commonly affecting terminal ileum and proximal colon, 90% premature babies
The aetiology of Necrotising Enterocolitis is a multifactorial exaggerated immune response within immature bowel. Give four risk factors
Prematurity
Hypoxia
Polycythaemia
Hyperosmolar milk feeds
NEC normally presents in the second week after birth, give three early and three late features.
Early: Vomiting, Poor Feed Tolerance, Distension
Late: Abdominal Tenderness, Blood/Mucous in stool, Shock
As well as a full range of bloods, an AXR will be carried out for NEC. Give three features
Gas in the gut wall (Pneumatosis Intestinalis)
Intestinal Distension
Gas outlining falciform (football sign)
NEC is staged using examination and radiological features via Bell Staging. Outline stages I-III
I - Suspected NEC
II - Proven NEC
III - Advanced NEC
How should feeding be managed in NEC?
Stop milk feeds for 10-14 days and insert NG tube
Start TPN
What is the definitive management of NEC?
Antibiotics for 10-14d (Benzylpenicillin, Gentamicin, Metronidazole)
Surgery if perforation/deterioration despite treatment/obstruction secondary to strictures
Surgical repair can be primary if localised disease, if extensive then resection and enterostomy followed by reanastamosis
Define Tracheoesophageal Fistula and state it’s associations
One or more fistulae communicating between normal trachea and oesophagus
Associated with VACTERL, CHARGE and trisomy 13/18/21
Define VACTERL Syndrome
Vertebral Defects
Anorectal Malformations
CVS Defects
TOF
Oesophageal Atresia with or without TOF
Renal Abnormalities
Limb Deformities
Defined when >3
What is CHARGE Syndrome?
Coloboma
Heart Defects
Atresia Chonae
Retarded Development
Genital Hypoplasia
Ear Abnormalities
How does TOF present Antenatally?
Polyhydramnios
Absent foetal stomach bubble
USS
How does TOF present post natally?
RDS
Choking
Frothing
Feeding difficulties
Name two investigations for TOF
AXR - curled NG tube, air in stomach
Fluoroscopy (swallow contrast)
Describe the five types of TOF
A - Pure Oesophageal Atresia
B - Oesophageal Atresia with proximal TOF
C - Oesophageal Atresia with distal TOF
D - Oesophageal Atresia with proximal and Distal TOF
E - H type (no atresia)
How are the non E type TOF repaired?
Pre-op bronchoscope followed by open thoracotomy
Fistula ties off
Anastomoses of oesophagus created
How are the E type TOF (H) repaired?
Surgery formed via neck
Risk of recurrent laryngeal nerve damage
Give four causes of Small Bowel Obstruction in Neonates
Atresia/Stenosis of Duodenum
Atresia/Stenosis of Jejunum/Ileum
Malrotation with Volvulus
Meconium Ileus
Give two causes of Large Bowel Obstruction in Neonates
Hirschsprung
Rectal Atresia
Define Omphalocoele and its presentation
Abdominal contents protrude through umbilical ring covered with transparent sac, often associated with other congenital abnormalities
Presents as a raised maternal AFP and 4-12cm Abdo wall defect
What’s the management for Omphalocoele?
Replacement of sac into abdominal cavity followed by closure
If the sac ruptures it’s treated the same as Gastroschisis
If larger it is enclosed in silastic sac and contents are gradually returned
Caesarean necessary
What is Gastroschisis and how does it present?
Abdominal contents herniate into amniotic sac with NO peritoneal covering
Presents as an opening less than 5 cm to the right of the umbilical cord
How is Gastroschisis managed?
There is a great risk of dehydration and protein loss so the abdomen should be wrapped in several layers of clingfilm
Most sorted with primary closure
If larger it is enclosed in silastic sac and contents are gradually returned
Vaginal delivery may be attempted
Define Meconium Aspiration Syndrome
Spectrum of disorders characterised by varying degrees of RD following aspiration (occurring either antenatally or during birth)
Describe the pathophysiology of MAS
Normally post term babies due to hypoxic stress leading to gasping
Results in obstruction (?Atelectasis), Hypoxia, Pulmonary Inflammation, Infection, Surfactant Inactivation, PPH
Give three risk factors for MAS
Gestational Age >42 weeks
Oligohydramnios
Thick Meconium
Describe 5 investigations for MAS
Chest a ray (patchy opacity, consolidation, increased lung volumes)
Infection Markers
ABG
Dual Pulse Oximetry (on RUL and LLL to determine shunts)
Cranial USS
Give three differentials for MAS
Transient Tachypnoea of the Newborn
Persistent Pulmonary Hypertension
Surfactant Deficiency
How is MAS is managed?
O2 therapy (extent depends on severity)
Antibiotics (stopped after 48 hours if culture is negative, eg ampicillin/gentamicin)
Potentially surfactant, or inhaled NO
Give three complications of MAS
Air leak (Meconium causes alveolar hyperdistension leading to pneumothorax)
Cerebral palsy
Persistent Pulmonary Hypertension
Define Transient Tachypnoea of the Newborn
Delayed clearance/absorption of lung fluid after birth, often after caesarean section.
Managed with oxygen and spontaneously resolves within 24 hours
Describe the CXR of TToN
Streaky perihilar changes
Fluid in horizontal lung fissures
Define Bronchopulmonary Dysplasia
Form of chronic lung disease affecting infants born preterm with oxygen requirements at 36 weeks
Impaired alveolar development with mechanical/oxidative/inflammatory factors
Give three risk factors Bronchopulmonary Dysplasia
Gestational Immaturity
FH of Asthma
LBW
How does the CXR present for Bronchopulmonary Dysplasia?
Hyperextended chest with diffuse patchy collapse and fibrosis interspersed by radiolucent cystic areas
Give five managements for Bronchopulmonary Dysplasia
Caffeine Citrate for premature
Oxygen
Diuretics
Corticosteroids
Immunisation against RSV
Describe the pathophysiology of Persistent Pulmonary Hypertension of the Newborn
Failure of the normal circulatory transition occurring after birth, causing R-L shunting and severe hypoxia
Can be Idiopathic, due to Diaphragmatic Hernia, or constricted vasculature due to RDS/MAS
How is Persistent Pulmonary Hypertension of the Newborn managed?
Treat underlying cause
Oxygen
Dopamine
Inhaled Nitric Oxide
Retinopathy of Prematuriy is the leading cause of preventable blindness. Who is most at risk?
Infants born at <32 weeks or weighing <1500g
Describe the pathophysiology behind Retinopathy of Prematurity
In utero retinal development occurs in a relatively hypoxic environment
Incompletely developed if premature and the hyperoxic environment can cause vasoconstriction and retinal ischaemia
Retinopathy of Prematurity can be classed by Severity and Location. Describe the stages of Severity
1 - Demarcation line visible
2- Ridge evident
3 - Ridge with fibrovascular proliferation
4 - Subtotal retinal detachment
5 - Total Retinal Detachment
Retinopathy of Prematurity can be classed by Severity and Location. Describe the stages of Location
Zone 1 - 30 degree radius from optic disc
Zone 2 - Nasal Regina periphery in circle
Zone 3 - circumference includes temporal and nasal retina
What does ‘+’ disease mean in Retinopathy of Prematurity
Engorgement of Posterior Vessels
Iris Rigidity
Vitreous Haze
When are infants screened for Retinopathy of Prematurity?
<27 weeks - screen at 30 to 31 weeks
27-32 weeks - screened at day 28 to 35 of life
Screen fortnightly unless plus/stage three disease
How is Retinopathy of Prematurity managed?
Diode Laser Treatment within 72 hours alongside steroid eye drops
Can be retreated if no regression at 10-14d
Name three causes of Vitamin K Deficiency (and subsequent HDN)
Breast Milk
Maternal Anticonvulsants
Newborn liver disease
Describe the presentation of mild and severe HDN
Mild - Bruising, Haematemesis, Malaena
Severe - Intracranial Haemorrhage
How is HDN prevented?
IM Vitamin K immediately after birth
If mother is on anticonvulsants then they receive an extra dose at 36 weeks
Describe the pathophysiology behind Intraventricular Haemorrhage
Related to rapid alterations in blood flow (eg severe RDS, hypoxia)
Bleeding can dilate ventricles and cause periventricular infarction due to compression
How do Intraventricular Haemorrhages present?
Most occur within 72 hours and 50% are asymptomatic
Larger bleeds can present with bulging fontanelle, neuro dysfunction, jaundice
Intraventricular Haemorrhages are seen on Cranial USS. Who should be screened and when?
At risk or pre term infants
At one day, one week and one month
The management for Intraventricular Haemorrhage is supportive. How can it be prevented?
Antenatal steroids and Indomethacin
Give two complications of Intraventricular Haemorrhage
Periventricular infarction
Post haemorrhage ventricular dilation (leading to CSF accumulation and raised ICP)
Describe the difference between Subgaleal and Cephalohaematoma
Subgaleal - boggy swelling all over scalp
Cephalohaematoma - subperiosteal bleed limited by suture lines
What is Periventricular Leucomalacia?
Softening the white matter associated with extreme prematurity (poor perfusion)
Visible on USS as Periventricular echodensities
Increased risk of cerebral palsy
What is Cleft Lip?
Failure of fusion of frontonasal and maxillary processes (can be unilateral or bilateral)
What is Cleft Palate?
Failure of fusion of palatine processes and nasal septum
Give two environmental and one syndromic cause of Cleft Palate
Foetal Alcohol Syndrome, Folic Acid Deficiency
Pierre Robin Syndrome
Apart from an obvious deformity, how could Cleft Lip/Palate present?
Difficulty feeding
Upper airway obstruction
Frequent Otitis Media
Spina Bifida is failure of midline fusion of dorsal vertebral bodies. What are the three types?
Occulta - no herniation, overlying dimple of hair
Meningocoele - herniation of meninges and fluid with a skin covering
Myelomeningocoele - involvement of neural tissue causing paralysis, incontinence etc
Milia is an example of benign neonatal dermatology, what are they?
<2mm yellow/white spots
Normally on face
Secondary to blocked sweat glands
Erythema Toxicum is an example of benign neonatal dermatology, what is it?
Discrete erythematous maculopapular lesions often with a white centre
Mostly over knees/elbows/trunk/face
Harlequin Colour Change is an example of benign neonatal dermatology, what is it?
Marked erythema/pallor in different halves/quadrants due to vasomotor immaturity
Superficial Capillary Haemangioma is an example of benign neonatal dermatology, what is it?
Also known as Stork Mark
Erythematous Vascular marks on eyelids/face/scalp/nose
Mongolian Blue Spots is an example of benign neonatal dermatology, what are they?
Bluish black machines often in lumbosacral region
Mostly non Caucasian
What is Nappy Rash?
Usually contact dermatitis from ammonia in urine
How would you manage simple nappy rash
Frequent nappy changes
Barrier Cream (Zinc)
When would you suspect a secondary infection of nappy rash? How would you manage?
Flexural or Satellite lesions
Topical Nystatin
What is Infantile Seborrhoeic Eczema? How is it managed?
Commonly affecting face/neck/behind ears/scalp
Normally resolves in weeks
Avoid detergents and give mild emollient and steroid
State the five parameters of the APGAR score
Activity
Pulse
Grimace
Appearance
Respiratory
How is ‘Activity’ of APGAR scored?
0 - none
1- flexed limbs
2 - active
How is ‘Pulse’ of APGAR scored?
0 - no pulse
1 - <100
2 - >100
How is ‘Grimace’ of APGAR scored?
0 - floppy
1 - minimal response
2 - prompt response
How is ‘Appearance’ of APGAR scored?
0 - Blue
1 - Blue Extremities
2 - Pink
How is ‘Respiratory’ of APGAR scored?
0- none
1 - slow and irregular
2 - vigorous
