Neonatology Flashcards
1
Q
What maternal factors indicate high risk pregnancy?
A
Unbooked
Antepartum bleeding
Maternal comorbidities - eclampsia, GDM, renal disease
Age
Infections
Substance abuse
2
Q
What fetal factory’s indicate high risk pregnancy?
A
Multiple gestation
Congenital malformation
Prem
Intrauterine growth restriction
Poly/oligohydramios
3
Q
What labour and delivery factors indicate high risk pregnancy?
A
Abnormal CTG
Prolonged ROM
Cord prolapse
Meconium stained liquor
Emergency c/s
General anaesthesia
Abnormal presentation
Prolonged labour
4
Q
What temperature should the delivery room be?
A
24-26 degrees celcius
5
Q
What temperature must a newborn be kept?
A
36,5-37,5 degrees celcius
6
Q
What position must you place the baby in to maintain the airway and what can help you do this?
A
Sniffing position
Towel under shoulders
7
Q
Who should be suctioned?
A
ONLY if obvious obstruction to spontaneous breathing - must be under direct vision
NOT routinely done
8
Q
What methods are used to provide positive pressure ventilation?
A
Bag Mask ventilation
AMBU (artificial breathing manual unit)
9
Q
When would you intubate a newborn?
A
Ineffective mask ventilation
Chest compressions required
Prolonged ventilation
Special circumstances eg CDH
10
Q
How do you determine the depth the tube must be inserted?
A
Weight(kg) + 6cm = depth (cm)
11
Q
How do you verify correct ETT placement?
A
Symmetrical chest rise
Misting of tubes
Auscultation
HR and colour improvement
12
Q
What are the tube sizes used for neonates?
A
<1000g = 2.5
1000-2000g = 3
2000-3000 = 3,5
3000-4000 = 3.5/4
13
Q
What is the ratio of compressions to breathes in resus of neonates?
A
3:1
14
Q
What is the dose and concentration of adrenaline in neonatal resus?
A
IV: 0,1-0,3ml/kg of 1:10000 adrenaline
ETT: 1ml/kg of 1:10000 adrenaline
15
Q
What and how much fluid is used for volume expansion in newborn?
A
10ml/kg of isotonic crystalloid (NS) /blood IV over 5-10mins
16
Q
If you have a poor response to volume expansion and adrenaline in resus of newborn, what next?
A
Consider pneumothorax
Check glucose : 2-4ml/kg 10% dextrose solution IVI
17
Q
What composes post-resus care of the newborn?
A
Maintain normothermia
Consider therapeutic hypothermia in hypoxia ischaemic encephalopathy
Monitor vitals and glucose
Transport to neonatal unit in closed incubator
Document resus
Inform parents
18
Q
What are the cardiovascular changes that occur after the first breathe?
A
①↓ pulmonary vascular resistance
② No flow through ductus venous
③ ↓ systemic resistance (no more low pressure placenta)
④ reversal of shunt through foreman ovale
⑤ reversal of shunt through ductus arteriosus
19
Q
What factors are considered in the APGAR score?
A
HR
Respiratory
Colour
Tone
Response to stimulation
20
Q
What are RF for birth injury?
A
Assisted delivery
Abnormal presentation
Precipitous delivery
Prematurity
Macrosomia
21
Q
Define birth injury
A
Traumatic event at birth causing structural/functional destruction of the neonates body
22
Q
Categorise birth injuries
A
Soft tissue
Cranial injuries
Nerve injuries
Fractures
Intra-abdominal injuries
Sub conjunctival haemorrhage
23
Q
What kind of soft tissue birth injuries occur?
A
Eccymosis and bruising
Petechiae (localised vs generalised)
Subcutaneous fat necrosis
Lacerations
Erythema and abrasions
24
Q
What kind of cranial brith injures occur?
A
Extracranial
- moulding
- cephalhaematoma
- caput
- subapomeurotic bleed
Intracranial
- subdural haemorrhage
- epidural haemorrhage
- subarachnoid haemorrhage
- intraventricular haemorrhage
25
Which extracranial injury is a medical emergency and how is it managed?
Subaponeurotic haemorrhage.
Monitor haemaglobinuria, serial head circumference, vitals
Supportive management - paracetamol for pain relief
Volume resus if shocked/transfusion
Check for jaundice as bleed is resolved
26
What nerve injuries occur during birthing?
Phrenic
Facial
Brachial
27
What fractures are common during birth?
Clavicle
Cranium
Humerus
Femur
28
What are some minor abnormalities commonly seen in the first few days of life?
Club foot
Vaginal discharge/ hymen tags
Vaginal bleeding
Peripheral cyanosis
Subconjunctival haemorrhage
Epstein pearls
Umbilical hernia
Breast enlargement
Positional talipes vs club foot
Negus simplex
Negus flammeus
Milia and miliaria
Erythema toxicum neonatorum
Transient pustular melanosis
Dermal melanosis
Transient vascular phenomena
Sucking blisters
Neonatal teeth
Gingival cysts
Polydactyly
Preauricular skin tags
29
Define neonatal hypoglycaemia
Glucose measuring <2,6mmol/l
30
Signs/sx of neonatal hypoglycaemia
Jittery/irritable/high-pitched cry
Lethargic/decreased consciousness
Hypotonia
Apnoea
Seizures
31
Risk factors for neonatal hypoglycaemia
Antenatal: maternal diabetes, maternal obesity, maternal B-blocker use
Neonatal: intrauterine growth restriction, prem, large for GA, sepsis, iatrogenic (no feeds/fluids), polycytaemia, HIE, hypothermia, rhesus allo-immune disease
32
What are the causes for PERSISTENT hypoglycaemia?
Hyperinsulinaemia
Endocrine deficiency eg GH deficiency, adrenal insufficiency
Inborn errors of metabolism
33
What investigations do you do in persistent hypoglycaemia?
Serum glucose
Serum insulin
Serum cortisol and GH
Sonar of adrenals
34
How do you manage neonatal hypoglycaemia?
Prevention: early feeding
Asymptomatic/glucose 1,4-2,5: enteral feeds
Symptomatic/glucose <1,4: IV bolus 10% dextrose followed by continuous infusion
Specific management depending on cause
35
What is neonatal encephalopathy?
Disturbed neurological function in the earliest days of life in infants born >/= 35 weeks GA
36
How does a patient with neonatal encephalopathy present?
Abnormal state of consciousness (hyper alert, irritable, lethargic, obtunded)
Decreased spontaneous movements
Poor tone/abnormal posturing
Absent/partial primitive reflexes
Difficulty initiating and maintaining respiration
Feeding difficulties
Seizures
37
What are the causes of neonatal encephalopathy?
Meningitis
Hypoxia ichaemic encephalopathy
Withdrawal from maternal “drugs”
Neonatal epilepsy syndromes
Genetic
Metabolic disorders
Structural brain abnormalities
Intraventricular haemorrhage
Non-accidental injury
Perinatal stroke
38
What are the abnormal signs consistent with hypoxia ischaemic encephalopathy?
Apgar <5/10 at 5 and 10 minutes
Foetal umbilical artery acid acidaemia (pH <7 or base deficit >12 or both)
Presence of multi organ dysfunction (brain, bone marrow, heart, lungs, kidneys, intestine)
Neuroimagining evidence of acute brain injury (deep gray matter and peri-Rolandic motor cortex)
39
What do you do when a patient has abnormal signs consistent with acute hypoxia encephalopathy?
Modified sarnat score
Or
Thompson score
40
What sentinel events are RF for suspected HIE?
Maternal
>cardioresp arrest
> impaired O2 eg asthma/PE
> hypovolaemic shock
Foetal
> exsanguination
• foetal maternal haemorrhage
• twin-twin transfusion syndrome
> cardiac arrhythmias in-utero
Uteroplacental
>abruptio
> cord prolapse
> ruptured placenta
>Hyperstimulation with oxytocin drugs
CTG patterns
>absent variability + recurrent late/variable decal. / Brady
> foetal tachy + recurrent decel
41
What is jaundice?
The yellow discolouration of the skin, sclera and mucus membranes
42
How do you determine the serum bilirubin?
NOT clinical
Non-invasive transcutaneous bilirubin
Or
Total serum bilirubin
43
Categorise jaundice
Unconjugated - indirect (fat soluble)
Conjugated - direct (water soluble)
44
Categorise the pathological causes of increased RBC destruction in unconjugated jaundice
Allo-immune
> Rh incompatibility
> ABO incompatibility
> minor antigen incompatibilities
Non-immune haemolysis
>RBC membrane defects
>RBC haemaglobinuria defects
>RBC enzyme defects
45
Categorise the non-pathological causes of increased unconjugated bilirubin production
Intravascular
>increased RBC breakdown (shorter RBC lifespan)
Extravascular
>bruising
>cephalhematoma
>subaponourotic bleed
46
What is the exception with regards to blood group antibodies and what problem does this cause?
All blood groups have IgM antibodies but group O has IgG antibodies.
If mom is group O, her anti A and anti B IgG antibodies can cross the placenta and cause haemolysis of the fetal blood.
47
How does Rh incompatibility work?
This requires sensitisation unlike ABO incompatibility.
First pregnancy: mom Rh neg and baby Rh pos = mom forms anti Rh IgG antibodies.
Second pregnancy: Moms anti Rh IgG antibodies cross placenta and attack fell Rh positive blood.
48
What are examples of hereditary RBC membrane defects?
Hereditary spherocytosis
Hereditary elliptocytosis
49
What is an example of RBC haemaglobinuria defects a.
Alpha thalassemia.
50
What are two examples of RBC enzyme defects?
Glucose 6 phosphate dehydrogenase deficiency
Pyruvate kinase deficiency
51
What investigations would diagnose intravascular haemolysis?
Haemaglobin decreased
Reticulocyte count increased
LDH increased
Haptoglobin decreased
RBC fragments on smear
52
What are causes of decreased hepatic uptake and conjugation of bilirubin?
Physiological
>immature liver enzymes needed for conjugation
>decreased net hepatic uptake
Pathological
>breast milk jaundice
>hypothyroidism
>Gilbert’s disease
>crigler-Najjar syndromes type 1 and 2
53
What are causes of increased henterohepatic circulation in unconjugated jaundice?
Pathological
>breast feeding failure
>meconium lieu’s
>hirschsprungs disease
>intestinal atresia
54
Main categories of causes of unconjugated hyperbilirubinaemia
Increased RBC destruction
Decreased hepatic uptake
Increased enterohepatic circulation
55
How do you investigate neonatal jaundice?
① total bilirubin+ conjugated bilirubin
= calculate unconjugated
② intravascular haemolysis? (Rh/ABO/non-immune)
• No » extravascular
• yes → direct Coombs test
③ positive direct Coombs = rh/abo incompatibility
negative = membrane /haem/ enzyme defects
56
How do you decide if it is pathological or physiological jaundice?
Refer to table 1
57
When is phototherapy contraindicated and why?
Conjugated hyperbilirubinaemia -> causes bronze baby syndrome
58
What are the indications for phototherapy?
Absolute
>see phototherapy chart
Prophylactic
>ELBW Iinfants
> extravascular bloood collections
>severe bruising, cephalhaematoma, IVH
59
What are complications of phototherapy?
Impaired bonding
Increased insensible water loss (older lights generate heat)
Watery stools
Maculopapular skin rash
Lethargy
Potential for retinal damage
60
How does phototherapy work?
It converts unconjugated bilirubin which is fat solvable into a harmless water solvable molecule which can be excreted in the urine and bile
61
What are the types of phototherapy?
Fluorescent tubes
Halogen bulbs
LED lights
62
When do you use a lower line for exchange transfusion?
If there is sepsis, haemolysis, acidosis or asphyxia
63
What are the indications for exchange transfusion?
① TSB > 85 above exchange threshold at presentation and not expected to fall below within 6hrs
② TSB remains above exchange line despite 6 hrs of intensive phototherapy
③ any acute signs of bilirubin encephalopathy
④ TSB rising quickly despite intensive phototherapy (>17umol/L per hour)
64
How does exchange transfusion works.
Removes maternal antibodies, and replaces87% of newborns blood with new blood. The bilirubin is removed from the plasma.
The blood for exchange is fresh, irradiated and reconstituted whole blood from packed RBC Oneg and FFP (AB)
Exchange double the volume
>160ml/kg term and 180ml/kg preterm
>5ml/kg at a time (max 20ml) with each cycle +- 2 mins
>venous umbilical catheter is ideal
65
Complications of exchange transfusion
Hypocalcaemia
Hypoglycaemia
Hyperkalaemia
Vasospasm and arrhythmias
Bleeding
Infections
Graft vs host disease
Hypothermia
Volume overload
66
What is the last option to treat unconjugated hyperbilirubinaemia aside from phototherapy and exchange transfusion? Why is it used?
IV immunoglobulin
Exchange transfusion has high risk complications. IVIG reduces rate of haemolysis and therefore reduces need for exchange transfusions.
Still needs more evidence
67
What are complications of prematurity?
-RDS
-retinopathy of prematurity
-PDA
-necrotising enterocolitis
-risk for hypothermia
-intraventricular haemorrhage
-apnoea of prematurity
-chronic lung disease of prematurity
-metabolic bone disease of prematurity
68
What strategies are used to prevent MTCT according to the PMTCT guidelines?
1) minimise infant exposure to virus by suppressing maternal VL
2) post exposure prophylaxis of the infant
69
What are the principles of infant prophylaxis at birth?
Principle 1: risk of baby determined by the VL of the mom at birth
Principle 2: infant is high risk until proven low risk
Principle 3: Continue prophylaxis until moms VL is suppressed
70
What determines high vs low risk neonate?
High risk = VL>1000 at birth or in last 12 weeks OR unknown VL
Low risk = VL<1000
71
What is high risk vs low risk prophylaxis according to PMTCT guidelines?
Low risk = Nevirapine once daily x 6 weeks regardless of feeding choice then cotrimoxazole until PCR negative >6 weeks after breastfeeding cessation and infant clinically HIV negative.
High risk = Nevirapine once daily x 12 weeks minimum + AZT twice daily x 6 weeks in the breastfeeding infant
Nevirapine x 6 weeks in the exclusively formula fed infant then cotrimoxazole
72
What does Breastfeeding Plus refer to?
It refers to infant feeding in the context of HIV. Integration of nutrition, nurture and medical intervention.
73
How long is exclusive breastfeeding recommended for?
First 6 months after which introduction of nutritionally adequate complementary feeding initiated.
74
When is breastfeeding NOT recommended?
A mother failing 2nd or 3rd line ART regimen.
75
What are the explanations for a baby testing positive during breastfeeding period?
1) Mom unsupressed (noncompliance/resistance)
2) False negative PCR at birth (birth PCR only tests for intrauterine transmission)
3) maternal seroconversion during breastfeeding
4) baby not fully tested previously
76
What measures are in place to identify and treat infected children as soon as possible?
Birth PCR
10week PCR
6 month PCR for HIV exposed infants
18 month Rapid/Elisa for ALL children (aligned with 18month maternal VL)
Thereafter, when indicated (when symptomatic)
6 weeks post BF cessation
77
How do we care for HIV exposed, negative children? What are they at risk of?
Follow up growth and development
Symptoms of anaemia
Poor birth outcomes
Maternal illness or death
History of hospitalisation
78
How frequently do pregnant women need to be tested for HIV?
At confirmation of pregnancy
At every antenatal visit
At birth
79
When do breastfeeding women need to be tested for HIV?
Every 3 months throughout breastfeeding
80
When must someone who has been exposed to HIV be tested?
Immediately
6 weeks post exposure (window period)
3 months post exposure
81
What is the 90-90-90 goal?
90% of the HIV population should know their status
90% of HIV positive patients who know their status should initiate ARV’s
90% of those who initiated ARV’s should have a suppressed VL
82
What is the modified sarnat score, what does it consist of and what is it used for?
It is a scoring system used to grade HIE (normal, moderate or severe encephalopathy) and decide if the patient qualifies for therapeutic hypothermia.
3 out of 6 categories are required
LOC
Posture
Spontaneous activity
Tone
Rimitive reflexes (Moro and suck)
Autonomic system (pupils, HR, Resp)
83
What is the Thompson score, what does it consist of and what is it used for?
It is used to score a baby to determine its risk of HIE.
Consists of:
1) limb tone
2) LOC
3) visible fits
4) posture
5) Moro
6) grasp
7) suck
8) resp effort
9) fontanel
Each category is given a score of 0-3. You add up the score at the end,
0=normal
1-10 = Mild
11-14 = moderate
15-22 = severe HIE
84
What are the long term neurodevelopmental sequelae of HIE?
Epilepsy
Cognitive impairment and developmental delay or learning difficulty
Blindness/vision defects
Cerebral palsy
Gross motor and coordination problems
Behavioural problems
Hearing loss/deafness
85
What multi organ involvement is expected in HIE?
Respiratory - PPH, Resp failure
Brain - seizures
Cardiac - hypotension, arrhythmias, ischaemia
Hepatic - elevated liver enzymes, coagulopathy
Bone marrow - thrombocytopenia
Renal - acute kidney injury
GIT - necrotising enterocolitis
Metabolic - hyponatraemia, hypocalcaemia, hypoglycaemia, hyperglycaemia
86
What are the neuroimagining patterns and correlating clinical pathologies in HIE?
GA 26 - 36 weeks = ishaemias → p-eriventricular white matter » spastic diplegia
GA > 36weeks =
1) partial asphyxia's event » parasaggital watershed areas +/- cortex = behavioural problems, language delays, cognitive deficits, possible epilepsy
2) acute total asphyxia → deep gray matter + perirolandic cortex = dyskinetic cp, spastic quad cp, cognitive impairment
87
How do you identify a baby with hypoxia ischaemic encephalopathy?
There is no gold stand diagnosis (most clinical signs/investigations are non-specific)
Abnormal signs consistent with HIE
Contributing events in close proximity to labour and delivery of RF
Long term neurodevelopmental outcome
88
What contributing events are RF for HIE?
Preconception
- advanced maternal age
- family history seizures/neuro disease
- infertility tx
- previous neonatal death
Antepartum
①fetal
- multi gestation.
- genetic abnormality
- congenital malformations
- IUGR
- breech
② maternal
- prothrombotic disease
- thyroid disease
- severe pre-eclampsia /chorioamnionitis
- antepartum haemorrhage
-trauma
Intrapartum
- abnormal fetas HR
- thick meconium
- assisted vag delivery
- emergency c/s
- abnormal lie
- shoulder dystopia
- abruptio
-GA
Postnatal
- 2° to pulm/cardio/ neuro disease
89
What is the management of HIE?
① supportive
- ABC
- glucose nb
- normothermia
- fluid restriction
- monitor for seizures (phenobarbital, phenytoin, lorazepam)
②neuroprotective
- therapeutic hypothermia (decrease progression of injury)
90
What is the MOA of therapeutic hypothermia?
↓ 2° cell damage
- a cerebral metabolism + energy utilisation
- inhibits inflammatory cascade
- suppresses free radical activity
91
What are the criteria for therapeutic hypothermia?
Must be <6hrs of life AND GA >36weeks
Physiological criteria:
-5 + 10 min APGAR <5
Or
-Ph < 7 or base def > 16
Or
Ongoing birth rhesus >10 mins
Neurological criteria:
-Moderate - severe on modified Sarnat +/- abnormal Thompson score
92
How do you diagnose conjugated jaundice?
Conjugated bilirubin >20% of total serum bilirubin
93
What enzyme converts unconjugated bilirubin to conjugated bilirubin?
UGT (glucuronosyltransferase)
94
What are the pathological causes of conjugated bilirubinaemia?
① infections
- torches
- parvovirus B19
- HIV
- sepsis (GBS, staph)
② Metabolic / genetic
- galactosaemia
- cystic fibrosis
- tyrosenaemia
③ endocrine
- hypothyroidism
- hypopituitism
④ Allo immune
- gestational allo immune liver disease (GALD)
⑤toxins
- drugs (inh)
- parental nutrition
⑥ Miscellan
- Idiopathic neonatal hepatitis
95
What liver enzymes indicate hepatocellular cause of conjugated jaundice and what ratios?
Increased ALT and AST
By 2-10 times
96
What are the cholestatic causes of conjugated hyperbilirubinaemia?
Extrahepatic
- biliary atresia
- biliary -cysts
- choledocal stones
- tumor /mass
- Neonatal sclerosing cholangitis
Intrahepatic
- alagille syndrome
-Intrahepatic biliary atresia
97
What are the clinical findings of conjugated jaundice?
Encephalopathy
-raised ammonia
-Hypoglycaemia
Cataracts
-metabolic disease
-congenital infection
Bleeding
-coagulopathy
Failure to thrive
-advanced liver disease
- sepsis
-metabolic disease
Portal hypertension
-dilated abdominal veins
-splenomegaly
-ascites
Acholic stools and dark
-obstructive jaundice
Firm hepatomegaly
-biliary atresia
98
How do you manage conjugated jaundice?
- Fat solvable vitamin supplementation (AEDK)
- MCT oil (medium chain triglyceride)
- Adequate calories
- Promote bile excretion (urodeoxycholic acid)
- Galactose is (avoid lactose containing feeds)
- Surgical - extrahepatic biliary atresia, cholodocal cysts and stones, masses
99
What are the complications of conjugated jaundice?
Increased PT and PTT
Albumin
Ammonia
Glucose
100
What investigations are done for suspected hepatic cause of conjugated jaundice?
LFT = elevated AST and ALT
- infections
- GALT
- A-1-AT
-thyroid functions
-serum ferritin
-sweat test/fecal elastase
101
What investigations do you do to investigate conjugated/obstructive jaundice?
Urine
-dipstix -> bilirubin
-pale stool
Abdo u/s
-presence of gallbladder
-extrahepatic bile ducts
-choledochal cysts or stones
-bile sludge
102
Which type of PCKD presents in the neonatal period?
Autosomal recessive
Dysfunctional kidneys
Multicyctic dysplastic kidneys with cysts in the renal parenchyma
103
What are examples of CAKUT?
Bilateral
-posterior urethral valve
-bladder neck obstruction
Unilateral
-posterior pelvoureteric junction obstruction
-vesicoureteric junction obstruction
104
How do you detect CAKUT?
Kidney sonar antenatally
105
What is a posterior urethral valve?
A mucosal fold that obstructs urine flow leading to hydronephrosis
-key hole appearance
-thickening of bladder wall
106
How is hypernatraemic dehydration managed?
1) calculate fluid losses and replace slowly over 24-48hrs
2) slow rehydration with a reduction in the sodium level by 0,5-1mmol/L per hour
Reduction faster = cerebral oedema
107
List 4 causes of Hyperkalaemia
1)increased administration
2)congenital adrenal hyperplasia
3) kidney injury/Impairment
4) haemolysis tube specimen
108
What is the most common bacterial infection in the neonate?
UTI
109
RF for UTI in neonates
1)prematurity
2) Caucasian
3) congenital abnormalities of the kidney and urinary tract
110
What is important to investigate when you diagnose a UTI in a neonate?
Sonar for exclusion of CAKUT NB
111
What are the 3 most common organisms that cause UTI in neonates?
E.coli
Klebsiella pneumonia
Enterobacter spp
112
What is optimal nutrition in infants?
1) exclusive breastfeeding for 6 months
2) complementary feeding (nutritionally adequate and safe) from 6months of age with continued breastfeeding up to 2 years of age
113
What is exclusive breastfeeding?
Infant receives breast milk only and no other liquids or solids (including water) with the exceptions of oral rehydration solution, vitamin/mineral supplements and medication.
114
What are the benefits of exclusive breastfeeding for 6 months?
-PMTCT
-provides all nutritional needs for first 6 months of life
-benefits increase with amount and duration of breastfeeding
-far lower risk of death from diarrhoea c9mpared to partial BF/formula
-reduces risk of diarrhoea and resp illness compared with exclusive BF 3-4 months only
115
What beneficial factors are in breast milk?
ANTI INFECTIVE FACTORS
-immunoglobulins (IgA)
-white blood cells (lymph, neutrophils, macrophages)
-whey protein (kills pathogens)
-oligosaccharides (prevent bacterial attach,ent to intestinal mucosa)
GROWTH FACTORS
-epidermal GF (intestinal mucosa)
-GF’s for development and maturation of nerves and retina
116
What are the benefits of breast feeding for the mother?
SHORT TERM
-decreases risk PPH
-bonding with baby
-milk is FREE, convenient, readily available
-accelerate recovery pre-pregnancy weight
LONG TERM
-delay return of fertility
-decreases risk of breast and ovarian cancer
-decreased risk DM T2, HT, hyperlipidaemia, CV disease
117
Benefits of breastfeeding for infant?
SHORT TERM
-ideal nutrition
-healthy weight gain
-milk easily digested
-maintains GI integrity
-immunity (less severe and common infections)
-decreased risk SIDS
-6-10x less likely to die in first months of life
LONG TERM
-less immunological diseases (asthma, DMT1)
-better cognitive fxn
-less obesity
-less CV risk in adulthood
-lower childhood leukaemia risk
118
What are medical reasons for using breast milk substitutes?
Baby
-different nutritional needs eg galactosemia
-in addition to breast milk eg hypoglycaemia
-separation from mother
mom
-maternal illness
-maternal medication eg radioactive iodine
-substance abuse
-HIV with high VL on 2nd line tx
119
What is the target feed volume for infants?
Term = 150ml/kg/day
Prem = 160-180ml/kg/day
120
What is the calorie requirements for neonates?
Prem = 120-150kcal/kg/day
Term = 100kcal/kg/day
121
Who are supplements given to and what supplements are given?
Iron
Vitamin D
Multivitamin
Given to preterm babies once on full feeds as they don’t have adequate iron stores,rapid growth (osteopenia of not supplemented)
122
What factors promote lactation and milk production?
-empty breast
-frequent feeding
-calm environment
-medication
123
What factors inhibit lactation/milk production?
-engorged breasts
-stressful environment
-pain, illness
-medication
124
What are the consequences of poor breast attachment?
-breast engorgement (not enough milk removed) = pain, blocked ducts, mastitis
-cracked and painful. Ipples
-refusal to feed
-insufficient milk intake
-oversupply of milk
125
What are the signs and sx of Candida in the mother and baby?
Mom
-painful breasts. It relieved between feeds
-red/flaky rash on areole with itching and depigmentation
Baby
-oral thrush
-refusal to feed or feed for short time
126
How do you treat Candida infection in mom and baby?
Nystatin suspension QID after breastfeeds
Nystatin cream to nipples after feeds
No need to tx mom of only baby symptomatic
127
How does a UTI present in a neonate?
YOU NEED A HIGH INDEX OF SUSPICION
(Any neonate with sepsis)
-poor weight gain
-vomiting
-pyrexia
-poor feeding
-lethargy
-diarrhoea
-prolonged jaundice (NB)
128
How do you investigate a UTI in a neonate?
GOLD STANDARD = single pathogen culture
-in out catheterisation
-suprapubic aspiration
-Blood = infective markers (CRP, high/low White cell count)
Urine dipstix - leukocytes may be negative due to frequent voiding
129
How do you manage a neonatal UTI?
-Start antibiotic tx (start B-road spectrum empirically until culture results are out)
-Repeat urine culture after 48hrs of antibiotics
-Renal u/s for every baby to exclude CAKUT
130
Define acute kidney injury
An abrupt decline in the ability to clear waste and to maintain fluid and electrolytes homeostasis
131
What parameters do you use to diagnose AKI?
-increase serum creatinine by 0,3G/dl
-increase serum creatinine by 1.5times the baseline
-UO <0,5ml/kg/hr for 6hours
132
How is AKI classified?
RIFLE
Risk of renal dysfunction (inc creat 150%)
Injury of the kidney (increased creat 200%)
Failure of kidney function (inc creat by 300%)
Loss of kidney fxn (>4weeks)
End stage kidney disease (>3 months)
133
What are the causes of AKI?
Prerenal (decreased blood flow to glomeruli)
-hypovolaemia
-blood loss
-decreased CO
-HIE
Renal
-congenital renal abnormality
-vascular insult (Renal vein thrombosis)
-nephrotoxins
-infection
-uncorrected prerenal
Post-renal (obstructive causes
-congenital obstructive uropathy
-neurogenic bladder
134
How do you investigate AKI?
-extensive history (underlying cause)
-examination = fluid status, UO, vitals
-Lab = U&E, CMP, urine analysis
-u/s and Doppler
135
How do you manage AKI?
Supportive
-fluid balance
-correct electrolytes and acidosis
-treat hypertension
-avoid nephrotoxin agents
-NB nutritional support (avoid high potassium and phosphate foods)
Persistent and severe = refer to nephro
136
When do you worry about undescended testes?
If they have still not descended by 6 months and definitely before 2 years = refer to surgery
137
What is the pathology of an inguinal hernia?
Continued latency of processes vaginalis = intermittent injuinal swelling
Not reducible = urgent surgical - risk of strangulation and incarceration
138
What is the pathology of a hydrocele and how is it managed?
Peritoneal fluid passes through the processes vaginalis and surrounds the tests (often bilateral)
Management
Resolves spontaneously, no management needed.
139
What are the 3 criteria for hypospadia?
Dorsal hood
Ventral chordee
ventral opening of urethra
140
What is the pathophysiology of congenital adrenal hyperplasia?
Deficiency in 21 hydroxylase enzyme leading to
- increased testosterone production
-decreased cortisol
-decreased aldosterone
141
What are the resulting effects of congenital adrenal hyperplasia? Ie clinically
-decreased cortisol = hypoglycaemia, adrenal crisis in periods of increased stress
-decreased aldosterone = Hyperkalaemia, hyponatraemia
-increased testosterone = virilisation of affected females (enlarged clitoris, ambitious genitalia) and males (darkening of scrotal area, enlarged penis)
142
What happens in salt losing adrenal crisis?
Vomiting, weight loss = circulatory collapse +/- hypoglycaemia
Hyponatraemia and Hyperkalaemia
143
What is the management of salt losing adrenal crisis?
Supportive
-fluids
-correction of electrolytes
-21 hydroxylase levels
-refer to endocrine for steroid replacement
144
How do you classify/approach a vomiting neonate?
Bilious vomiting = intestinal obstruction until proven otherwise
Non-bilious =
1) intestinal obstruction
2) non-obstructive
145
What are causes of non-bilious vomiting?
Obstructive
-duodenal/pyloric stenosis
-annular pancreas
Non-obstructive
-physiological (over feeding)
-infection
-CNS (ICP)
-endocrine
-drugs
-cows milk protein allergy
146
What are the causes of bilious vomiting?
ALWAYS PATHOLOGICAL
Intestinal obstruction
-Functional = Hirschprungs, ileus
-anatomy = small/large bowel atresia, imperforate anus
147
What is the difference between vomiting vs regurgitation?
Vomiting = active, involuntary, forceful expulsion
Regurgitation = passive, effortless progress which happens without force
148
What is the management of vomiting neonate?
Stabalize and rehydrate (serial weighing to monitor hydration)
Investigate underlying cause
-FBC (infection?)
-X-ray abdo
-electrolytes (hypochlorite is = pyloric stenosis)
-urea and creat
-blood culture
Treat underlying cause
149
How do you approach a neonate with abdominal distension?
1) intestinal obstruction (functional or mechanical -upper/lower GIT)
2) Ileus
3) pneumoperitoneum (intestinal perforation)
150
How do you manage an ileus?
Check K (hypokalaemia can worsen the paralysis)
Rest bowel - NPO
NG tube with free drainage to decompress
ID and treat underlying cause
151
How do you manage a pneumoperitoneum?
NPO
Insert NG tube on free drainage to decompress
General stabalisation (ABC)
Surgical consult for definitive tx (laparotomy/pencil drain)
152
How does an UGIT obstruction present?
Hx: polyhydramnios
Early vomiting
May/may not pass meconium
Abdo distension may develop later
153
How does LGIT obstruction present?
Abdominal distension
Delayed/absent passing of meconium
Vomiting = late feature
154
What is the most common type of oesophageal atresia?
Proximal atresia with distal oesophageal fistula with trachea
155
How would oesophageal atresia present?
Polyhydramnios
Increased Frothy secretions
Choking
Cyantoic spells
156
How do you diagnose oesophageal atresia?
NG tube. CXR shows coiling of the NG tube
Or barium swallow
157
How does duodenal atresia presents?
-bilious/non-bilious vomiting
-feeding intolerance in first 48-72 hours
158
What findings on the X-ray for duodenal atresia?
Double bubble sign
159
What syndrome is associated with duodenal atresia?
Trisomy 21
160
How does pyloric stenosis present in a neonate?
-projectile vomiting 3-8weeks postnatally
-vomit towards the end of feed
-olive-like mass in right upper quadrant with visible peristalsis
161
What investigations would you do and what would the findings be of pyloric stenosis?
U&E - hypokalaemic, hypochloraemic metabolic alkalosis
Ultrasound
162
How do you treat pyloric stenosis?
Surgical management/referral
163
What would you see on the X-ray in ileal/jejunal atresia?
Triple bubble sign
164
What are the differences between gastroschisis and omphalocele?
Gatroschisis = defect in abdominal wall with herniation of contents which are not covered by protective layer
Omphalocele = gut doesn’t rotate and failure of gut to return into the abdomen
Gastroschisis = associated abnormalities rare
Omphalocele is associated with other conditions (trisomy 13, 18 and Beckwith Weidemann)
Gatroschisis = right paraumbilical
Omphalocele = central
Gastroschisis = no sac covering
Omphalocele = covering sac
Gatroschisis = free intestinal loops
Omphalocele = liver, bowel, etc
Gastroschisis = excellent prognosis if managed well (and small)
Omphalocele = Varies with associated anomalies
Gastroschisis = immediate management = cover bowel with cellophane to reduce fluid losses, IV fluids, NG tube, antibiotics, urgent surgery
Omphalocoele = bowel covered by sac, semi-urgent surgery unless sac rupture then tx for gastroschisis
165
What history is important to ask in a neonate with respiratory distress?
Antenatal
-preterm or poster, delivery
-maternal drugs
-maternal illness
-chorioamnionitis
-oligo/polyhydramnios
Perinatal
-meconium liquor
-PROM
-fetal distress
-difficult delivery
-assisted delivery
Postnatal-excessive drooling
-requiring oxygen
-hypoglycaemia
-coughing/choking when feeding
-resus needed?
166
What is the pathophysiology of cleft lip/palate?
Failure of closure of the lateral and medial nasal processes during the 8th week
167
What are complications of cleft lip/palate?
Short term
-feeding difficulties (need dental plate and special nipples)
Long term
-middle ear infection
-hearing impairment
-speech difficulties
-facial growth and orthodontic problems
168
How is cleft lip/palate managed?
Surgical repair of lip - 3months
Palate repaired 6-12 months
169
What is the inheritance pattern of Pierre Robin syndrome?
Single gene defect and is autosomal recessive
(X-linked variant involved cardiac malformations and clubfoot)
170
What is the aetiology of Pierre Robin syndrome?
7 and 11th week - mandibular hypoplasia
Tongue kept high in oral cavity causing a cleft and preventing closure
Inverted U-shaped cleft and absence of associated cleft lip.
171
What is the Pierre Robin syndrome triad?
Micrognathia
Posterior palate defect
Tongue posterior leg displaced (retroglossoptosis)
172
What is a complication of Pierre Robin syndrome?
Resp obstruction = hypoxia = cor-pulmonary = pulmonary HT
173
What is the management of Pierre Robin Syndrome?
Prevent obstruction by tongue (prone, may need CPAP via NG tube)
Micrognathia and airway obstruction improve in 2 years
Surgery of palate around 1 year
174
What is choanal atresia?
Bony/membraneous blockage between the nasal cavity and nasopharynx which can be uni/bilateral
175
Why is choanal atresia a problem?
Newborns are obligatory nose breathers so it can be life threatening causing resp distress and cyanosis, relieved by crying or opening the mouth
176
How do you diagnose Choanal atresia?
CT scan
NG tube/nasal airway unable to pass
177
How is choanal atresia treated?
Establish airway (oral airway)
Surgical correction by ENT’s ASAP
178
How do you approach respiratory distress?
Respiratory
1) pulmonary
-RDS
-TTN
-Congenital pneumonia
-pulmonary haemorrhage
-pneumothorax
-congenital lung disease
2) non-pulmonary
-upper airway problems
-lower airway problems
-diaphragm pathologies
-mediastinal masses
-rib cage abnormalities
Non-respiratory
-cardiac
-metabolic
-neuromuscular
-haemolytic
179
What investigations would you order in Resp distress of the neonate?
FBC + diff
CRP
Blood culture
CXR
Cranial and renal u/s
CTscan
180
What are signs of respiratory distress?
Tachypnoea >60
Nasal flaring
Grunting (prolonged exp against closed glottis)
Chest retraction
-suprasternal
-sternal
-inter/subcostal
Cyanosis
181
What are the findings on a CXR with RDS?
Ground glass appearance
Air bronchograms
Low lung volumes
182
What is important history in a neonate with RDS?
Prem?
Gets DM?
Meconium asp? (Decreases surfactant activity)
183
How do you treat RDS?
AN steroids (prevention)
CPAP
Surfactant
184
What is the most common cause of resp distress in term infants?
Transient tachypnoea of the newborn
185
What is the pathophysiology of TTN?
Lower circulation of catecholamines = Na channels not activated in c/s causing delay in the absorption of lung liquid
186
What is the management of TTN?
Oxygen
NG feeding
CPAP
Roma
Resolves within 24hrs about
187
When might an infant get meconium aspiration?
>34-36 weeks GA (meconium not present before)
188
What is the pathophysiology of meconium aspiration?
Causes inflammatory response (chemical pneumonitis = obstruction and atelectasis = over distension = alveolar rupture, pneumothorax, surfactant deactivation = PPHN
189
What factors promote passage of meconium in utero?
Placental insufficiency
Hypoxia
Maternal HT
Preeclampsia
Maternal drug abuse
Oligohydramnios
190
What are complications of meconium aspiration?
Airway obstruction
Surfactant dysfunction
Chemical pneumonitis
Pneumothorax
Persistent pulmonary HT of the newborn
191
What are X-ray features of meconium aspiration?
Course, widespread patchy infiltrates with hyperinflation
192
What is the management of meconium aspiration?
Prevention
Mechanical ventilation with high flow (NO CPAP = worsens hyperinflation)
Surfactant support
Ionotropes
193
What are risk factors for congenital pneumonia?
Chorioamnionitis
PROM
Maternal fever/tachy
Hx UTI/vaginitis
Spontaneous ROM
194
What is the most common causative organism of congenital pneumonia?
Group B strep
195
What are the X-ray findings of congenital pneumonia?
Bilateral opacities,
Focal infiltrates with air bronchograms
196
What is the treatment of congenital pneumonia?
Antibiotics (Ampicillin)
Ventilation if signs of resp failure
197
List the causes of persistent pulmonary hypertension of the newborn.
Birth asphyxia
Meconium aspiration
Sepsis
Diaphragmatic hernia
198
What is the CXR features of PPHN?
Oligaemia (decreased vascularity)
May be normal
may show underlying cause
199
How does a neonate with PPHN present?
Cyanosis or difficulty in oxygenation
Reduction between pre and post duct all saturations
200
What is the management of PPHN?
Oxygen
Optimise mechanical ventilation
Circulatory support required
Consider surfactant therapy
Pulmonary vasodilator (NO inhaled)/oral or IV sildenafil
201
How is a hyperoxia test conducted?
Predictably ABG done on RA
100% O2 given for 10 minutes
PaO2 >110mmHg = unlikely cyanotic heart disease
PaO2<110mmHg = likely cyanotic heart disease
202
What rash is this in picture7?
Erythema toxic neonatorum
203
What rash is this (figure 8)?
Ache neonatorum
204
What rash is this? Image 9
Transient neonatal pustular melanosis
205
What is the rash in image 10?
Seborrheic dermatitis
206
What is happening in image 11?
Transient vascular phenomena (cutis marmorata)
- transient mottling of the skin symmetrically involving trunk and extremities
207
What is happening in image 12?
Transient vascular phenomena (harlequin colour change)
When newborn lies of his sides (blanching of contra lateral side)
Resolves with increased muscle activity or crying
208
What is the distribution of erythema toxicum neonatorum?
Palms and soles spared.
Lesions on face, trunk, proximal extremities
209
Describe a typical erythema toxicum neonatorum lesion.
2-3mm maculae’s and Paula’s that evolve into pustules and are surrounded by blotchy erythema. =flea-bitten appearance
210
What infections have a similar appearance to erythema toxicum neonatorum and should be kept in mind?
Candida
Herpes simplex
Staph infections
211
How do you confirm diagnosis of erythema toxicum neonatorum?
Pustular smear
Eosinophilia
212
Describe the appearance of transient neonatal pustular melanosis rash.
Lack surrounding erythema
Lesions rupture easily leaving collarette of small and a pigmented macula that fades over a few weeks.
213
Identify the rash in image 13.
Milia
214
What’s the difference between miliaria crystallina and miliaria rubra?
Miliaria cyrstallina = caused by superficial eccrine gland duct closure, 1-2mm vesicles without erythema
Miliaria rubra = caused by deeper eccrine gland obstruction, erythematous papules and vesicles on portions of the skin
215
How is seborrheic dermatitis treated?
White petrolatum
Tar containing shampoo (often on scalp)
Hydrocortisone
216
What is the distribution of seborrheic dermatitis?
Scalp “cradle cap”, face, nappy area, ears, neck
217
What lesion is in picture 14?
Negus flemmeus/ Port wine stain
218
What is the triad of Sturgeon-Weber syndrome?
Seizures
Glaucoma
Port wine stain
219
Port wine stain in the __________ distribution is of the _______ nerve is associated with ______________.
Opthalmic
Trigeminal
Ipsilateral glaucoma
220
What is the lesion in image 15?
What is it caused by?
Negus simplex
“Stork bites”/ “angel kisses”
Caused by telangiectasis in the dermis
221
What’s the difference between neonatal sepsis and congenital infections?
Neonatal sepsis requires rapid and empiric antibiotic treatment and progresses fast, presents early
Congenital infections can be asymptomatic at birth and progress variantly and result in poor long-term outcomes.
222
What are the differences between early onset sepsis and late onset sepsis?
Early onset = presents <72hrs of life
Late onset = presents >72hrs of life
Early onset = transplacental, genital tract/PROM transmission
Late onset = nosocomial, HCW, community/environment, nutritional resources, immature immune system
Early onset = GBS, EColi, listeria monocytogenes, staph aureus, h influenzas
Late onset = GBS, Staph aureus, fungal, enterococcus, gram neg organisms
223
Define neonatal sepsis
The presence of infections involving bloodstream, urine, CSF, peritoneum/any sterile tissue during the first 28 days of life
224
What are RF for Early onset neonatal sepsis?
Maternal factors
-prem labour <37 weeks
-PROM >18hrs
-chorioamnionitis/maternal fever >38
-GBs bacteruria
-colonised with GBS
Neonatal factors
-prem
-male
-low apgar
-hypothermia
-fetal distress
225
What are the RF for late onset sepsis?
Inversely related to GA and weight
Catheters
Ventilator tx
Prolonged AB
Damage to skin from tape/skin probes
Gastric acid suppression therapy
226
How does early onset neonatal sepsis present?
Non-specific symptoms
-temp irregularity
-change in behaviours
-skin = poor circulation, jaundice, mottling, umbilical redness/discharge
-GIT = vomiting, diarrhoea, abdo distension, jaundice
-Cardio/pulmonary = resp distress, tachypnoea, poor cap refil
-metabolic = hypo/hyperglycaemia
-CNS = irritability, abnormal cry, bulging fontanelle, lethargy, seizures, coma
227
What is the clinical presentation of late onset sepsis?
Neonatal meningitis (GabS)
Conjunctivitis
Pneumonia
Umbilical infection
UTI
Osteomyelitis/septic arthritis
Skin = impetigo, staph scalded skin syndrome
228
How do you investigate neonatal sepsis?
Thorough history and exam
Blood, urine, CSF, tracheal secretions = gold standard
**CSF for:chemistry, microscopy, culture, latex agglutination
CXR, AXR (NEC, pneumonia)
FBC
-leukopenia/leukocytosis
-neutropenia
-immature neutrophils:total neutrophil ratio >0,2
-platelet count
Acute phase reactants
-CRP
-procalcitonin
229
What is the treatment for neonatal sepsis?
1) Prevention (antenatal care, hand washing, infection control, management of catheters, BF, judicious use of AB)
2) Antibiotics (empiric = lifesaving)
-ampicillin and gentamicin for early onset sepsis, length of tx depends on disease progress)
-LOS tx depends on cause (vancomycin, cephalosporins, carbapenems, antifungals)
230
How do you judge how long you should give AB tx for?
Judge by clinical picture and by your CRP and other inflam markers
231
What organisms commonly cause congenital infections?
Viruses
-Rubella
-CMV
-HSV
-Varicella zoster
-hep B and C
-HIV
-enteroviruses
-papilloma virus
Bacteria, parasites etc
-toxoplasma Gondi
-trop pallidum
-mycobacterium tuberculosis
-plasmodium
232
How does CMV congenital infection present?
1) Asymptomatic (90% at birth)
2)Clinical signs:
-prematurity
-rash
-IUGR
-jaundice
-hepatosplenomegaly
Neuro manifestations
-microcephalic
-seizures
-hypotonia
-lethargy
-chorioretinitis
-intracranial calcifications
-sensorineural Hearing loss9
233
How do you diagnose CMV?
1) in mother
-seroconversion (neg IgG to pos IgG)
-CMV DNA PCR of amniotic fluid
2) in infant
-IgM (within 3 weeks of age)
-CMV viral DNA of blood, urine, amniotic fluid, saliva of CSF before 3 weeks)
234
How do you treat CMV infection?
No vaccine
Hygiene practice
IV ganciclovir 6 weeks 6mg/kg/dose
235
How does congenital rubella present?
1) asymptomatic at birth 2/3
2) Rubella syndrome
-sick baby
-jaundiced
-petechiae
-hepatosplenomegaly
-blueberry muffin rash
-thrombocytopaenia
-cataracts
-glaucoma
-hearing loss
236
How do you diagnose congenital rubella?
DNA PCR in nasopharyngeal swabs, urine, CSF, blood
Rubella specific IgM before 3%months
Rubella IgG between 6-12 months
237
How do you treat rubella?
No treatment available
Vaccination NB
238
How is toxoplasma Gondi transmitted to the baby?
Mom primary infection during pregnancy by raw meat/inhalation feline faeces
239
How does toxoplasmosis present?
Classic tetrad
-cerebral clarifications
-hydrocephalus
-chorioretinitis
-seizures
75% asymptomatic at birth
-maculopapular rash
-cataracts
-deafness
240
How do you diagnose toxoplasmosis?
PCR
IgM in amniotic fluid and newborn
241
How is toxoplasmosis treated?
Spiramycin in in 1st/early 2nd trimester
Pyrimethamine/sulfadiazine in late 2nd/3rd trimester and continue 1year post birth
242
How does congenital varicella syndrome present?
Varicella is teratogenic
-foetal loss
-IUGR
-skin scarring
-limb deformities
-eye and CNS abnormalities
243
How does the timing of moms infection of varicella influence the neonate?
Any stage = IUGR/neonatal infantile zoster
1st 20 weeks = congenital varicella syndrome
>5-6days before delivery = neonatal varicella at age 10-12 days
<4-5 days before to 2 days after delivery = neonatal varicella from birth -12 days after delivery (insufficient t8me for maternal IgG development and passage to fetus
244
How do you treat neonatal varicella? NB
Varicella zoster Immune globulin
Aciclovir for I’ll neonates
Vaccinate moms 3months prior to pregnancy
245
How does a mom present with syphillis and why is it important to identify?
Primary stage (3-6weeks) = painless, spont resolving petechiae
Secondary stage (6-8weeks) = diffuse inflammation and a disseminated rash often on palms and soles
Latent stage = asymptomatic
Infection occurs in the neonate when the mom is untreated or inadequately treated therefore prenatal care NB
Early infection = hydrous fetal is, stillbirth, prem, LBW, neonatal death
246
How does congenital syphillis present in a child?
Early (<2years)
-prem and growth restriction
-hepatosplenomegaly
-nasal chondrites
-skin rash
-osteochondritis
-neurological symptoms including hydrocephalus
Late (>2years)
-craniofacial abnormalities
-dental abnormalities
-deafness
-neuro syphillis
-frontal bossing
-sabre skin
-cognitive disability
-interstitial keratitis
247
How do you investigate congenital syphillis?
Screen infant - nontreponemal serologic testing = non-specific but quant and qualitative
-VDRL
-RPR (rapid plasma regain test)
Treponemal tests (positive if past infection)
-enzyme immunoassays
-fluorescent trep antibody absorption = FTA-ABS
248
How do you treat congenital syphillis?
Treat mother fully
Treat infant
1)asymptomatic
-benzathine penecillin 50000 u/kg stat IF MOM received less than 3 doses, mom delivers within 4 weeks of tx
2)symptomatic
-procaine penecillin/benzyl penecillin for 10 days
Erythromycin doesn’t cure !!!
249
What are the RF of HIV transmission to child?
Maternal Unsuppressed viral load
Prem
Unknown RVD status
Mixed feeding
PROM
Vag delivery
250
What is the fixed dose combination used to treat HIV in pregnant women?
TLD
Tenofovir (TDF)
Lamivudine (3TC)
Dolutegravir (DTG)
251
What are the benefits of using dolutegravir?
Rapid viral load suppression
High genetic barrier to resistance
No interaction with hormonal contraceptives
SE minimal
252
What are the cons of using dolutegravir?
Small risk neural tube defect
Drug interactions (rifampicin, metformin)
253
What are the benefits of using efavirenz?
Safe in pregnancy
No interaction TB tx
254
What are the risks of using Efavirenz?
Low genetic barrier to resistance
Drug interaction with contraceptives
Neuropsychiatric SE
255
How do you assess a treated patient with a viral load >50?
Adherence
Bugs
Correct dose
Drug interactions
E resistance
256
How is prematurity classified?
Late preterm = 34-36weeks 6days
Moderate preterm = 32-34weeks
Very preterm = 28-32 weeks
Extreme preterm = <28weeks
257
What factors can you look at to determine the babies age/GA?
Birth weight
Skin
Vision
Ears
Hearing
Sucking and swallowing
Cry
Feeding
Taste
Breathing
Breast tissue
Sleep/wake cycle
Posture
258
How do you classify weight at birth?
Large birth weight = >4kg
Low birth weight = 1500-2499g
Very low birth weight = 1000-1499g
Extreme low birth weight = <1000g
259
Between what percentiles is “normal” weight for ages? What does it mean if you are above or below?
10th-90th percentiles
Below = IUGR
Above = large for date
260
Further classify IUGR
Symmetrical
-length, weight and HC small for age
Asymmetrical
-weight small but HC and length normal for age
261
Classify small for GA
Constitutionally small (reached genetic potential)
IUGR
262
How is delayed cord clamping beneficial?
Fluid bolus (cardiovascular stability)
Reduce Intraventricular haemorrhage
Reduce necrotising enterocolitis
Reduce need for vasopressin’s and blood transfusions
NB not if baby needs resus
263
What are the golden rules of prem delivery
Prevent hypothermia
Prevent hyper/hypoxia
Noninvasive ventilation
Early enteral feeding
Delayed cord clamping
Prevent hypoglycaemia
Early admin AB
264
How do you prevent hyperopia in a prem?
Titration the oxygen supplementation using pulse oximetry to guide you
Term = infatuate 21%
Preterm = initiate 21-30%
And monitor response
265
What are the complications of prematurity?
Intraventricular haemorrhage
Retinopathy of prematurity
RDS
PDA
NEC
Infection
Anaemia
Coagulopathy
Jaundice
Poor weight gain
Electrolyte disturbance
Metabolic bone disease
266
Why are perms susceptible to hypothermia?
Unable to shiver
Less subcutaneous fat
Increased skin to volume ratio
Inability to take in enough calories
267
How do you keep a preterm neonate warm?
Put in plastic polyethylene bag, hat on head NB
KMC
Warm fluids
Humidified vent basses
268
What is the Pathogenesis of RDS?
Incomplete lung development and insufficient endogenous surfactant
No surfactant = collapse of alveoli on expiration and atelectasis = increased work of breathing
269
What is atelectasis?
Lung collapse
270
How do you diagnose RDS?
Presents within 4 hours after birth (when surfactant is used up
Clinically
-subcostal recessions/intercostal recessions
-tachypnoea
NB sternal recessions
-nasal flaring
-expiratory grunting (collapsed lungs)
CXR
-collapsed lungs
-disuse uniform ground glass appearance
-air bronchograms
271
How do you manage RDS?
Antenatal steroid administration
CPAP with supplemental O2
Monitor eats
If not tolerating, exogenous surfactant
272
What are complications of RDS?
Infection/lung collapse
Air leaks (pneumothorax/pulm interstitial emphysema)
PDA
Pulm haemorrhage
Intraventricular haemorrhage
Bromchopulmonary dysplasia
273
Define apnoea
Cessation of breathing for >20secs with bradycardia or hypoxaemia
274
What is the management of a PDA?
Fluid restriction
Diuretics (if signs of heart failure)
Prostaglandin synthase inhibitors (ibuprofen/paracetamol)
Surgical closure
275
What is NEC?
Process of inflammation of the bowel wall that may progress to necrosis and perforation
276
How does a patient with NEC presents?
Bloody stools (late sign)
Distended abdo wall veins, erythema
Abdo distension
Inability to tolerate feeds: vomiting/Bilious aspirates
Intramural air on X-ray = Intestinal perforation
Systemic signs NB!!!
-CNS - lethargy, irritability
-CVS = decreased peripheral perfusion, hypotension, shock
-resp = resp distress, bradycardia
-renal = oliguria, Andria
-metabolic = acidosis, hypo/hyperglycaemia, electrolyte abnormalities, jaundice, temp instability
277
What are the RF for NEC?
Prematurity (>>>)
BF is protective
Micro biome pattern of guy
278
How do you investigate NEC?
Bloods
-FBC
-Urea, creatinine, electrolytes
-serum bilirubin
-coagulation profile
-blood culture
-Abg
Radiology
-abdo X-ray = pneumatosis intestalis is pathognomonic (intramural air)
279
How do you manage NEC?
Stabilise (airway, breathing, circulation)
If resp support required, use invasive (diaphragm splinted)
Correct hypotension and acidosis, bleeding diathesis = vit K and FFP
Keep NPO (insert NG tube on free drainage)
Initiate broad spectrum antibiotics
280
What is the Pathogenesis of IVH?
Germinal matrix highly susceptible to damage as a result of alterations in blood flow/coagulation disorders as it is highly vascular
= damage of vascular network with varying degrees of bleeding
281
How does IVH present?
Typically asymptomatic
Diagnosed on screening sonar at 72hrs of age (advised in infants less than 32weeks GA)
Or
-abnormal neurological signs
-apnoea and bradycardia
-shock
-acute drop in Hb conc
-hyperglycaemia
-unexplained acidosis
-unexplained increasing vent support
282
How do you manage IVH?
Stabalise
Obtain cranial u/s
Refer for further management
283
What is retinopathy of prematurity?
Eye disease of prematurity caused by vasculopathy and abnormal proliferation of retinal bv = leaking and scarring and retinal detachment and then blindness.
284
Define chronic lung disease of prematurity
O2 requirement at 28 days of life
O2 requirement and characteristic X-ray changes at 28 days of life
O2 requirement at 36weeks postmentrual age
285
What supplementation must the preterm infant receive and for how long?
Iron
Vit D
Multivitamin
For 6 months
286
What factors cause delay in onset of respiration at birth?
Intrauterine hypoxia
Trauma to the brain
Drugs depressing resp centre
287
What is the effect on the baby if opioids are given to the mom, and how do you treat this?
Resp depression
Administration of nalaxone (opioid antagonist)
288
What is depicted in image 16?
Mongolian spot
289
What is indicated in image 17?
Stork bite/telangiectasic naevi in nape of neck
Disappear in first years of life
