Neonatal Medicine Flashcards
1
Q
What is respiratory distress syndrome and who is most at risk
A
Deficiency in surfactant
Prematurity (also babies of DM mothers)
2
Q
How does respiratory distress occur
A
- Insufficient surfactant leads to Atelectasis (lung collapse)
- Re-inflation with each breath exhausts baby causing respiratory failure
- Hypoxia from respiratory failure leads to decreased CO, hypotension, acidosis and renal failure
- Death - major cause of death from prematurity
3
Q
What are the signs of Respiratory Distress
A
Increased work of breathing shortly after birth Tachypnoea Grunting Hypoxia/Cyanosis intercostal regression Nasal flaring
4
Q
What will be seen on CXR with someone with respiratory distress
A
Diffuse granular appearance (ground glass appearance) +/- air bronchograms
5
Q
What are two differentials for respiratory distress
A
Transient Tachypnoea of the newborn - due to excess lung fluid usually resolves in 24hrs
Meconium Aspiration
6
Q
How is respiratory distress prevented
A
Betamethasone/Dexamethasone should be given to all women at risk of premature labour from 23-35 weeks
7
Q
How is Respiratory Distress Syndrome treated
A
- Delay cord clamping
- Give CPAP with a PEEP
- Persists: intubate with mechanical ventilation and O2 inhalation ( around 90% - 100% is toxic)
- ET tube administration of artificial surfactant within 2 hours of birth
- Supportive measures: IV fluid replacement, stabilisation of glucose and electrolyte levels
8
Q
What is bronchopulmnary dysplasia/chronic lung disease
A
Chronic lung disease primarily found in premature infants who have exposed to prolonged mechanical ventilation and O2 therapy for RDS
(still requiring ventilation at 36 weeks gestation)
9
Q
How does bronchopulmoary dysplasia occur and how will it present
A
Ventilation causes barotrauma, recurrent infections, pneumothorax, inflammation etc.
Continuance of S/S from RDS
10
Q
How is BPD diagnosed
A
CXR: fine granular densities
Histology: Necrotizing bronchiolitis, fibrosis and atelectasis
11
Q
What are the complications of BPD
A
Early: feeding problems, severe RSV bronchiolitis, GORD
Late: lowered IQ, cerebral palsy, pneumothorax
12
Q
What is meconium aspiration
A
In term/near term infants - when meconium in the fetal colon is passed in utero leading to meconium stained amniotic fluid (MSAF)
13
Q
What are the two causes of MSAF
A
Fetal maturity
Fetal Distress
14
Q
What can MSAF lead to
A
meconium aspiration - This leads to respiratory distress in the born infant
15
Q
What are the complications of meconium aspiration
A
Airway Obstruction
Surfactant disfunction
Pulmonary Vasoconstriction
Infection
16
Q
What is the Rx for meconium aspiration
A
- unresponsive neonate with green stained amniotic fluid - Emergency intubation and Endotracheal suctioning
- Surfactant
- Ventilation
- Inhaled NO
- Abx
17
Q
what is hypoxic Ischaemic Encephalopathy/ Asphyxia
A
Brain injury secondary to lack of oxygen/blood flow to baby
18
Q
What may cause hypoxic ischaemic encephalopathy/ Asphyxia
A
Antepartum, intrapartum, postpartum
- Cord prolapse
- Maternal Hypoxia e.g eclampisa/epilepsy
- Placenta Abruption
- Vasa Praevia
- Respiratory Distress Syndrome
19
Q
How may an infant with hypoxic ischaemic encephalopathy present
A
Varies on severity of hypoxia
- Respiratory Depression
- Need resuscitation
- pale blue skin
- slow/weak pulse
- acidosis
- hypotonia
- Encephalopathy develops within 24hrs of birth
20
Q
How is encephalopathy managed
A
- Resuscitation and Ventilation
- Fluid, Blood pressure and perfusion management
- Therapeutic Hypothermia - standard in term babies with moderate/severe HIE (reduces death and disability)
- Monitoring and Treating Seizures e.g general anaesthetic
21
Q
What are congenital TORCH infections
A
Pathogens transmitted from mother to child during pregnancy or delivery
22
Q
What are the TORCH infections
A
T oxoplasmosis O thers e.g syphilis, varicella, parvovirus B19 R ubella C ytomegaly H erpes Simplex Virus
23
Q
What can the TORCH infections cause
A
Spontaneous abortion
Premature birth
IUGR
CNS, endocrine, skeletal and organ abnormalities
24
Q
How does Toxoplasmosis present and how is it prevented
A
Classic Triad: Chorioretinitis, diffuse intracranial calcifications and hydrpcephalus
Also may get blueberry muffin rash
Prevention: Avoiding uncooked meat, avoiding handling cat faeces
25
How does Syphilis present and prevention
Jaundice, Hepatosplenomegaly, nasal discharge, maculopapular rash and skeletal deformities (later facial abnormalities)
Prevention: Treat mother with Penicillin
26
What does Varicella Zoster present with and how is it prevented
```
IUGR
premature birth
Cateracts
Encephalitis
Pneumonia
CNS abnormalities
```
Prevention: active immunisation of mother before pregnancy, passive immunisation with VZIG, Acyclovir
27
How doe parvovirus B19 present and how is it treated
Aplastic Anaemia
Fetal Hydrops
Prvention: Frequent hand washing, avoiding contaminated places e.g schools
28
What does rubella cause and how is it prevented
Petechiae and Purpura (blubbery muffin rash)
Sensorineual Deafness
Cateracts
Heart Defects
Active immunisation before pregnancy
29
What does the Cytomegaly virus present and how is it prevented
- Jaundice
- Hepatospelomegaly
- Sensorineural Deafness
- Petechiae and Purpura (blueberry muffin rash)
- Microcephaly
Prevention: Frequent handwashing and avoiding contaminated places, Valacyclovir
30
How does HSV present and how is it prevented
- Premature birth
- IUGR
- Skin, eyes and mouth involvement
- Meningitis
Prevention: C-section if disease active, Acyclovir
31
When should live vaccines be given
MMR or Varicella should be given 3 months before conception they are contraindicated in pregnancy
32
Why and when does Physiological Hyperbilirubinaemia occur
Common! - occurs AFTER 24hrs birth
ALWAYS unconjugated!
1. Increased bilirubin production due to shorter RBC lifespan
2. Decreased bilirubin conjugation due to hepatic immaturity
3. Absence of gut flora impedes elimination of bile pigment
4. Exclusive Breastfeeding - However continue breastfeeding!
33
What tests should you do for jaundice within 24hrs
FBC
Blood Film
Blood groups
Coombs Test - may be +ve in ABO incompatibility
34
What is prolonged jaundice and what are its causes
```
not fading after 2 weeks term or 3 weeks preterm
Causes:
- Breastfeeding
- Sepsis (UTIs, TORCH)
- Hypothyroidism
- CF
- Biliary Atresia if conjugated and pale stools
- Galactosemia
```
35
How is Jaundice treated
Phototherapy - light energy converts bilirubin to soluble products that can be excreted without conjugation
Exchange Transfusion
36
What can pathological jaundice be caused by in newborns
Conjugated HyperBilirubin
| Unconjugated HyperBiliruibn
37
What are the causes of conjugated Hyperbilirubin
```
Decreased bilirubin excretion
Intrahepatic Cholestasis
- SEPSIS
- Hep A and B
- TORCH
- CF
- Metabolic
Extrahepatic Cholestasis
- Billary Atresia
- Tumours
- Prolonged Parenteral Nutrition
- NEC
```
38
What are the causes of unconjugated Hyperbillirubin
Haemolytic
- Infection or Sepsis
- Haemolytic Disease of the Newborn e.g Rh disease, ABO incompatibility, RBC defects, G6PD Deficiency
Non Haemolytic
- Hyperbilirubinemia Syndromes
- Hypothyroidism
39
What is a complication of prolonged Jaundice
Unconjugated Bilirubin is lipid Soluble and can cross blood brain - high levels cause Kernicterus
(Conjugated high levels nothing to worry about)
40
How does Kerictierus Present
Acute Bilirubin Encephalopathy
- Lethargy
- Poor Feeding
- Hypotonia (floppy baby)
- Shrill Cry
- Apnoea
- Seizures and Muscle Spasms
Chronic Bilirubin Encephalopathy (yellow staining of brain)
- Cerebral Paresis,
- Hearing impairment
- Vertical gaze palsy
- Movement disorders
- Intellectual and Developmental Disability
41
What is oesophageal atresia and what is the most common form
congenital defect in which the upper esophagus is not connected to the lower esophagus, ends blindly instead
Esophageal atresia with a fistula connected distally to the trachea is the most common kind of esophageal malformation
42
What are the signs of OA
Prenatal:
Polyhydramnios
Small Stomach
Postnatal:
OA: Pooling of scecretions- excessive secretions and foaming from mouth
Tracheoesophageal fistula:
- Aspiration leading to Aspiration Pneumonia
- Cough
- Airway Obstruction
- Cyanosis
43
How is OA diagnosed
Inability to pass catheter into stomach
| X-ray - oesophageal pouch, no gas in abdomen
44
How is OA Rx
Stop feeding
Continuous Suction of secretions from Oesophageal pouch
Urgent Surgery
45
What is Gastroschisis and Exomphalus
How is it diagnosed
How is it treated
Gastroschisis: A birth defect of the anterior abdominal wall just lateral of the umbilical cord in which babies intestines are found outside the babies body
not covered in membrane - exposed to the air
Exomphalus: Abdominal contents protrude through abdominal wall through belly button but are covered in an amniotic sac formed from amniotic membrane and peritoneum (umbilical cord attached to sac)
Most commonly antenatally on US
Cover exposed bowel with clingfilm after delivery
Keep Baby warm and Hydrated
Close defect surgically as soon as possible
46
What is a complication of diabetes in the newborn
Hypoglycaemia - can lead to seizures and brain injury if prolonged
Caused by making too much insulin during pregnancy if mother has poorly controlled diabetes
47
How is hypoglycaemia managed
Monitoring blood glucose levels
Give formula or glucose water mixture
IV glucose if severe
48
How can Hyperthyroidism during pregnancy affect the fetus
High numbers of TSH receptor stimulating autoantibodies can cross placenta cause fetal thyrotoxicosis
(usually mothers with Graves Disease)
49
What can fetal thyrotoxicosis lead to
```
Fetus:
Premature Delivery (after 24 wks)
Goitre,
Extended Neck in labour
Fetal Tachycardia
```
Neonate:
Hyperthyroidism: irritability, restless, tachycardia, hyperphagia, poor weight gain, diffuse goitre, microcephaly
50
How does neonatal thyrotoxicosis usually manifest
- Straight after birth
| - 10 days later after transplacental maternal antithyroid medication has worn off!!
51
How is neonatal hyperthyroidism treated and what are complications if left untreated
Neonatal Graves disease resolves 1-3 mths
Symptomatic: Propanalol and Methimazole
Cardiac Failure
Intellectual Disability
Hyperactivity
52
Who and why is Neonatal sepsis most common in
Premature Babies
| Last 3 mths of pregnancy there is active transfer of IgG to fetus if premature they get less of it
53
How is Infection acquired to neonates
Transplacentally
Ascent from vagina
During Birth
Environment once born
54
What is sepsis and how does SEPSIS present
Dysregulated Host response to infection leading to end organ failure
Common causes: Meningococcal and Streptococcal
Non specific and subtle
- Temperature
- Lethargy
- Poor Feeding
- Respiratory Distress
- Collapse
- DIC - Jaundice
55
What and the RF and common causes of early onset neonatal sepsis
```
Early onset:
Prolonged ROM
Maternal Infection e.g pyretic, chorioamnionoitis
Mother carrier of group B Strep
Preterm Labour
Fetal Distress
Breaks in neonatal skin
```
Causes (aquired from mother): GBS, E.Coli, or Listeria, Herpes, Chlamydia
56
What are RF and common causes for late onset neonatal SEPSIS
```
Late Onset:
Central lines and Catheters
Congenital Malformation e.g spina bifida
Severe Illness
Malnutrition
Immunodeficiency
```
Causes (acquired from environment): Coagulase -ve Staphylococci, Staph Aureus, E.coli, GBS, Also BEWARE fungal SEPSIS from Candida should be considered in those who don't respond to normal therapy
57
How is neonatal SEPSIS managed
- ABCDE
```
Blood Cultures
Urine output
Fluids
Antibiotics
Lactate
Oxygen (94%)
```
- Do all these within the hour
- Appropriate Escalation (ICU)
58
How is Group B Haemolytic Strep transmitted and how does it present
Via Mothers vagina
Can present straight away or delayed (up to a month)
Can lead to Meningitis!!!
Give all Mothers high risk of passing GBS or +ve to GBS prophylactic IV BenPen throughout labour
59
What is the most common facial malformation
Cleft Lip and Palate
60
How does Cleft lip and palate occur
Failure of fusion of maxillary and premaxillary processes (defect runs from lip to nostril)
61
What can cause Cleft Lip and Palate
Genes
Benzodiazapines
Antiepileptics
Rubella
62
How can cleft lip and palate be prevented
Quit smoking
Folic Acid
Avoidance of anti epileptics
63
How is Cleft Lip and Palate treated
MDT: Orthodontist, Plastic surgeon, Oral Surgeon, GP, Paediatrican, Speech Therapist
Unilateral - good cosmetic outcome
Bilateral- will always be some residual deformity
64
What are complications of cleft lip and palate
Otitis Media
Aspiration
Poor Speech
Avoid taking to NICU - poor bonding
65
What is retinopathy of prematurity
Hyperoxic Insult (risk factors O2 therapy and prematurity)
- arrests normal vascular growth
- Fibrous ridge formations
- Abnormal Vascular proliferation
- Retinal Haemorrhages
- Severe: Retinal Detachment, Blindness
66
How is retinopathy of prematurity managed
Low risk changes - nothing, regular follow up
| High Risk changes - Later Therapy
67
What are the infant benefits of Breast Feeding
```
Less infection
Less immune driven/allergic disease: Cancer, Eczema, DM, Crohns, MS
Reduced risk of NEC
Reduced GORD
Higher IQ better cognition development
```
68
What are maternal benefits of Breast Feeding
Reduces risk of cancer: Endometrial, Ovarian, Breast
Improved Health: Postpartum Haemorrhage, Post partum depression, Osteoporosis, Child Abuse
Promotes post party weight loss
Less food/medical expense
Delays Fertilty
69
How is feeding managed in premature babies
IV fluids and Parenteral Nutrition
Trophic Feeding
Monitor Growth
Suck and Swallow starts 32-34 wks
70
What is Apnoea of prematurity
Brain Stem not fully developed baby forgets to breath also associated with bradycardia
71
How is Apnoea managed
Made worse by SEPSIS
Physical; NPAP, Stimulation
Drugs: Caffiene
72
What is in the newborn physical examination
Eyes - cataracts
Heart - heart murmurs
Testicles - descended?
Hips - check for DDH
73
What is IVH and who is it most common in
Bleeding inside or around the ventricles of the brain
Premature babies, VLBW - fragile vessels usually occurring in first 72hrs of life
74
How does IVH present and complications
- Apnoea
- Bradycardia
- Cyanosis
- Seizures
- Lethargy, Coma
- Blood clots occlude outflow from ventricles - Hydrocephalus
75
How is IVH managed and what are its complications
Supportive care of resuscitation, fluids and oxygen
Hydrocephalus/raised ICP - Surgery for Shunt
76
What is hydrocephalus and how does it present
Accumulation of CSF within the ventricles of the brain
- Raised ICP: vomiting, headache, papilloedema and coma
- Increased head circumference: skull sutures haven't fused yet
- Open anterior fontanel will bulge
- Severe: Failure of upward gaze (sunsetting eyes)
77
How is hydrocephalus managed
Ventriculoperitoneal shunt
| Extra Ventricular Drainage - acute and severe
