Neonate Conditions

Question 1

What is the retinopathy of a prematutiry

Answer 1

Developing retina.
RF: LBW & prematurity
Exposure to supplemental O2 is a cause. - careful saturation.
Abnormal fibrovascular proliferation of retinal vessels- may cause retinal detachment & visual loss.
There are 5 stages- extend of detachment.

Question 2

What is the tx of Detinopathy of prematurity?

How do u screen for it?

Answer 2

Diode laser therapy causes less myopia than cryotherapy.

Screen if

Question 3

What happens during the first breath? How can this be interrupted?How is pulmonary HTN achieved?

Answer 3

1st breath: pulm vasc resistance falls, blood in lungs. Partially mediated by Nitic oxide (NO) - fetal to adult circulation- interrupted by; meconium aspiration, pneumonia, resp distress syndrome, diaphragmatic hernia, group B strep infx and pulm hypoplasia.
Pulm HTN arises as a consequence of these events

Question 4

Whats primary pulmonary hypertension?

Answer 4

Pulm HTN arising from hypertrophy of the muscular layer of pulm arteries

Question 5

What do u do if u suspect pulm HTN? What helps?

Answer 5

See backround.. Eg cause.
Immediate echocardiograohy. If abscent of structural disease, R-to-left shunting of ductus arteriosus.
Inhalation of nitric oxide helps circulation and improve pulm outcoumes in preterms (1000-1250g) + ⬇️ risk of brain injury.

Question 6

How does iNO help?

Answer 6

Relaxes smooth muscle by ⬆️ production of cyclic guanosine monophosphate.
May also be assc w/ ⬆️ risk of IVH.
Alternative: adenosine, prostacyclin.

Question 7

How does ventilatory support for neonates work?

Answer 7

Improve O2 exchange, decrease work of breathinh,menanle ventilatiom for those w/ resp depressiom or apnoea.

Question 8

What are some non-invasive ventilation procedures?

Answer 8

🔹HNFC: high flow nasal cannula- +ve pressure on airays similar to CPAP- humidifying the gas delivered-⬇️ mucosal dryness. May reduce days compared to CPAp.
🔹CPAP- continuous positive airway pressure; + diff resp cycles. assisting spontaneous inspiration- few compl, 1st choice.
🔹NIPPV- nasal intermittent positive pressure ventilation- combines nasal CPAP with superimpost ventilator breathing at set pressure.
Used as a bridge between invasive and cpap.

Question 9

What are some of the procedures for imvasive ventilation?

Answer 9

🔶Conventional mechanical ventilation (CMV- intermittent mandatory ventil. IMV)
🔶High frequency ventilation.
🔹TCPL -time cycled pressure limited ventilation. Humidifyed and heated air Via ET (endotracheal) tube , nasotracheal siting best.
🔹PTV:patient- triggered ventilation- combines TCPL with sensor that detects spontaneous breaths. Then sends a breah that is synchronised with patient’s inspiration.
🔹HFV- high frequency ventilation- delivers small volumes of gas at a very rapid rate. Aim: to reduce ventilator assisted lung injuries. There are many types.

Question 10

What are some complications of mechanical ventilation of neonates?

Answer 10

Due ro the +ve pressure they produce, + pressures will cause some haemodynamic compromise (hypotension, ⬇️ cardiac output)
Lung: pneumothorax, pulm haem., bronchopulmonary dysplasia, interstitial pulm emphysema, pneumonia. Opportunistic: multidrug resistant organisms.
Airways: upper airw obstr- worse on inspiration- stridor.
Consider bronchoscopy- supraepiglitc lesions.,.
Others:
Patent ductus arteriosus, ⬆️ ICP, +/- IVH, retinopathy of prematurity

Question 11

What is neonatal intensive care?

Answer 11

ABC and E- for epithelial cells- determine whether low birth weight will survive putside the uterus.
They manage all ex utero world: lung mechanics/ gas exchange
Renal tubular disease,
Cold: small vol & large SA- allow much heat outside. Incubators!
Usually premature babies.

Question 12

When do we suspect IVH? What are some complications? How do u diagnose it?

Answer 12

Infants that deteriorate rapidly

Question 13

What happens in IVH? (Intravascular haem) who is at risk? What might reduce the risk?

Answer 13

25%

Question 14

Whats the normal heart rate for the fetus in the uterus?

Answer 14

110-160bpm.

Normal fetal heart rate

Question 15

What happens in hypoxic-ischaemic neinatal enceohalopathy?

Answer 15

⬇️PaO2, ⬆️PCO2, metabolic acidosis.
⬇️CO-⬇️ tissue perfusion= hypoxic ischaemic injury to brain and some organs.
↪️ Disability/death
Usually an ischaemic episode happens before or during labour. :
♦️F of gas exchange across placenta- Xs/ prolonged uterine contractions, placenta abruption, ruptured uterus.
♦️interruption of cord flow- cord compression- cord prolapse or shoulder dystocia.
♦️inadequate maternal placenta perfusion, maternal hypotension/HTN, often w/ IntraUterineGR
♦️compromised fetus-anawmia, IUGR
♦️F of cardioresp adaptation at birth- F to breathe.

CF- immediately or 48hrs after asphyxia.
Mild- irritable, respinds xs to stimulation, impaired feeding, starring of eyes, hyperventilation
Moderate-markd abbnormalities of tone + movement, cannot feed, may have seizures.
Severe- no normal spntaneous movements or response to pain. Limb tone may fluctuate between hypotonia and hypertonia.
Seizures are prolonged and often refractory to tx, until multi organ F.

1o neuronal death or 2o neuronal death- delayed from reperfusion injury–> offering opportunity for neuroprotection w/ hypothermia.

Question 16

How would you manage neonatal encephalopathy? Whats the prognosis?

Answer 16

Skilled resuscitation + stabilisation minimises neural damage. May need:
Resp supprort, aEEG- recording of amplitude-integrated electroencephalogram,- cerebral function monitor. To detect abn backround activity to confirm eaely encephalopathy or identify seizures.
Tx of clinical seizures with anticonvulsants.
Tx of hypotesntiom by vol + inotrope support.
Monitor + tx hypoglycaemia + el ctrolyte imbalance esp hypocalcaemia.

From 2009! Main tx!! Cryotherapy- mild hypothermia to 33-34 degrees (rectal temp) for 72hrs by wrapping infant in cooling blamket reduces brain damage if started within 6hrs of birth (thats the only window- glutamate excitation leaves the channels open- intracellular Ca2+ enters the neurons causing neural death).

Prognosis- mild- complete recovery expected.
Moderate but asymptomatic now- can feed by 2 weeks normally- excellent long term prognosis- if clinical abn resist beyond that time- full recovery unlike.
Severe-30-40% mortality, survivors-80% neurodegelopmental disability partic. Cerebral palsy.
MRI at 4-14 days- bilateral abn in basal ganglia and thalamus + lack of myelin in posterior limb of internal capsule- later cerebral palsy.
⭐️⭐️
Mild hypothermia for moderate and severe HIE reduces death and severe disability and incrases the likelihood of survival with normal neurological fx.

Question 17

Whats meconium?

Answer 17

Earliest stool passed by a mammalian infant.
Composed of material from uterus- intestinal epithelial cells, lanugo, mucus, amniotic fluid, bile + water.
Viscous + sticky like tar, dark olive green. Almost odorless.
Stools progress into yellow(digested milk) as the first days progress.
Usually retained into fetus’ bowel, sometimes
Expelled in amniotic fluid- meconium liquor
↪️ sign of fetal distress- risk of meconium aspiration.

Medical staff aspirrate meconium from nose or mouth. To prevent meconium aspiration syndrome.

Question 18

What are the causes of neonatal deaths?

Answer 18

57%immaturity
23% congenital abn
11% intrapartum causes
Infection-5%
4% other specific causes.

Question 19

What happens in birth injuries?

Answer 19

Malpositioned/ too large for pelvic outlet
Manual manoeuvre:forceps/ ventouse deliveries.
C/S ⬇️ these.,

Soft tissue injury-
Caput succedaneum- mesto derma- bruising + oedema of presenting part. - extends beyond skull bone margins; resolves in a few days.
- cephalohaematoma- haematoma from bleeding below periosteum- confined with margins of skull sutures- usually involes parietal bone. Centre of haematoma feels soft- resolves within several weeks.
- chignon- bruising and oedema from ventoude delivery- marginated.
- bruising after face presentation or buttocks after breech.
-preterm- bruise easy- mild trauma.
Skin abrasions- after scalp electrodes applied or scalpel inscision at C/S.

Nerve palsies

1. Brachial nerve palsy- (C5+C6) traction to bracial roots- breech or shoulder dystocia– erbs palsy.
2. If elevated diaphragm- accomp by phrenic neeve palsy.
3. Facial nerve palsy- facial n compressed at ischial spine of mother. Unilateral, facial weakness on crying, eye remains open, .
4. Rare- palsy due to cervical damage- weakness below lesion- lack of movement.

Fractures-
Clavicle- shoulder dystocia- no tx.
Humers-femur - tx- immobilisation.

Question 20

How does Erbs palsy look?

Answer 20

Affected arm lies straight, limp amd with hand pronated and fingers flexed. (Waiters tip position)

Question 21

How do palsys resolve?

Answer 21

Spntaneously by 2-3w. If not, refer to orthopaedic or plastic surgeon.
Most recover:2Y.

Question 22

What are some medical problems of preterm infants?

Answer 22

Esp 23-26w.
After 32w- excellent prognosis
Need for resuscitation at birth- HIE
Resp-RDS, pmeumothorax, apnoea& bradycardia (3mins)
Hypotension
Patent ductus arteriosus (L–>R)
Temp control (thinner skin ⬆️ heat radiation loss) , ⬆️SA/V ratio- lose heat.
Metabolic- hypoglycaemia(GDM), Hypocalcaemia (phosphate deficiency) , electrolyte imbalance, osteopenia of prematurity, nutrition,
infection,
jaundice,
necrotising entercolitis,
retinopathy of prematurity,
anaemia of prematurity( Fe transfer to fetus at 3rd tri- no time) ,
Bronchopulmonary dysplasia (requiring o2 past 36w post menstrual)
Inguinal hernias

Question 23

What happens in resp distress syndrome?

Answer 23

Surfactant deficiency, lowers surface tension.
1. Widespread alveolar collapse
2. Inadequate gas exchange
Common 60breaths/min.
Laboured breathing+ chest wall recession (sternal + subcostal indrawing) + nasal flaring.
Exp grunting- try creating +ve airway pressure during expiration + maint functional residual capacity.
Cyanosis of severe.
CXR- bilateral oneumothoraces

Tx- oxygen + surfactant- ⬇️ morbidity and mortality.
↪️ CPAP- nasal cannulae or artificial ventilation via tracheal tube.

Question 24

What is surfactant?

Answer 24

Surfactant- phospholipids and proteins- excreted by type 2 pneumocytes of alveolar epithelium

Question 25

Whats another bame for RDS? Why?

Answer 25

Hyaline membrane disease- due to proteinaceous exudate seen in airways on histology

Question 26

How would you manage RDS?

Answer 26

Surfactant from pig via tracheal tube- reduces mortality

ANC- glucocorticoids/ corticosteroids- stimulate surfactant production- given if preterm delivery anticipated.

Question 27

How would u stabilise a preterm/sick infant?

Answer 27

Airway/ breathing
- resp distress: tachypnoea, laboured breathing + chest wall recession, nasal flaring, expiratory granting, cyanosis.
Mx- clear airway, oxygen, high flow humidified oxygen, CPAP- continuous positive airway pressure) , mechanical ventilation.

Monitoring:
Oxyg. Sat- 88-95% if preterm- higher amounts are dangerous.
HR rate, (leads on limbs)resp rate, temp, BP, blood glucose, ABGs, wt.

Temp control- place in plastic bag- keep warm- if VLBW- cling film.
Under tadiant warmarer, or humidified incubator to avoid hypothermia. (Blanket on feet- feel like in uterus)

Venous and arterial lines:

1. Peripheral intravenous line- IV fluids + antibiotics + drugs.
2. Umbilical venous catheter- IV access at resuscitation, or meds needing central delivery (inotropes)
3. Arterial line- inserted if frequent blood gas analysis, blood tests, cont BP monitorring. Usually Umbilical artery catheter (UAC) . Arterial oxygen tension maint: 8-12kPa (60-90mmHg). Co2 tension (4.5-6.5kPa (35-50mmHg).
4. Central venous line for peripheral patenteral nutrition. - inserted when infant stable.

CXR w/ or w/o abdo XR.
Assists in dx of RDS- glass appearance + confirm position of tracheal tube + central lines.

Inv- hB, neutrophil count (leukopenia), platelet count.
Blood urea,creatinine, electrolytes and lactate( lactic acidosis)
Blood glucose- hypoglycaemia usually
CRP/ acute phase reactant
Coagulation screen if indicated.

Antibiotics- broad spec given early- if cultures negative, stop within 48hrs.
Minimal handling+ analgesia
Parents need to see it.

Question 28

What happens in a pneumothorax? How could you prevent one?

Answer 28

RDS-air from overdistended alveoli may track into interstitium-> pulmonary interstilial embolism (PIE) .
10% kids ventilated for RDS- air leans into pleural cavity –> pneumothorax- O2 req ⬆️ - chest sounds and expansion reduced of that side. Demonstrated- by transillimination w/ bright fibreotic light source applied to chest wall.

Tension pneumotharax- insert chest drain- 2-3rd ICS

Prevention- infants ventilated w/ lowest pressure.

Question 29

What do we do in apnoea, bradycardia and desaturation?

Answer 29

Brady: 3mins.
Stops breathing for 20-30s, or breathing against closed glottis.
Exclude other- hypoxia, infx, anaemia, electrolyte disturbance, hypoglycaemia, seizures, HF, asporation, GORD,
Mainly- immaturity of central resp control.

Breathing starts again after physical stimulation- caffeine.
If apnoeic episodes frequent- CPAP.

Normal HR- 110-160bpm. If moving tho, HR increases

Question 30

How do you go about temperature control?

Answer 30

Hypothermia- ⬆️ energy consumption–> hypoxia + hypoglycaemia, F to gain wt, ⬆️ mortality.
Preterms part vulnerable:
1. ⬆️ SA/V ratio- lose heat > heat generation.
2. Skin thin- Xs heat radiation out.
3. ⬇️ SC fat for insulation
4. Nursed naked- cant curl up or shiver to produce heat.

Prevention of heat loss:

1. Convection- raise temp of ambient air in inc. clothe, cover haed. Avoid draughts.
2. Radiation- cover baby, double walls for incubators.
3. Evaporation- dry and wrap at birth- verylowbirthweight- directly into plastic bag. Humidify incubator- avoid diffusion.
4. Conduction- nurse on heated matresses.

Question 31

What happens in a patent ductus arteriosus?

Answer 31

Most common in RDS infants.
Blood shunting from L-> R
CF- apnoea, bradycardia, no sx. Increased oxygen demand.

Invx- echo
Tx- ibuprofen ↪️
Prostaglandin synthase inhibitor-indometacin.

Question 32

Nutrition tips

Answer 32

Preterms- high nutritional req.

35-36w suck and swallow.

Question 33

Infx?

Answer 33

Infx- major cause of death (strep B) and contributes to bronchopulmonary dysplesia (chronic lung disease), white matter injury in brain + later disability. .

Preterm babes-
IgG tranferred across placenta in 3rd trimester, no IgA or IgM transferred.

Question 34

Whatbare some preterm brain imjuries?

Answer 34

VLBW hemiplagia.

Large intraventricular haem- may impair drainage + reabs of CSF - cSF build up– resolve or –> hydrocephalus–> causes cranial sutures to separate, head circumference increases rapidly- anterior frontanelle tenses. Tx- LP to relieve tension- or intraventricular shunt.

Question 35

What happems in mecrotising enterocolitis?

Answer 35

Mainly affecting preterms
Assc w/ bacterial infx of ischaemic bowel. + ones fed cows milk.
CF-
Stops tolerating food, milk aspirated from stomach + V- bile stained.
Abdo- distended, stool- fresh blood. Rapid shock –> artificial ventilatiom due to abdo distention and pain.

aXR- distended loops of bowel & thickening of bowel wall, w/ intramural gas (inside loop layers) or gas in portal tract. (In liver)
↪️ bowel perforation - detected on AXR or by transillumination of abdomen.

Tx- stop oral feeding, give broad spec antibiotics to cover anaerobes and aerobes.
Suegery for bowel perforation
Morbidiry + mortality-20%.

Long term compl- strictures develop, malabsorption if edtensives bowel resection done.
Parenteral nutrition Always needed- artificial ventil + circ support may be needed.

Question 36

Whats retinopathy of prematurity?

Answer 36

ROP- affects developing blood vessels developing at junctiom of vascular and non vascularised retina. Vascular proliferation may progress ro retinal detachment, fibrosis and blindness.

Risk- ⬆️ by uncontrolled use of high concentrations of oxygen.

Tx- laser therapy

Question 37

Whats the definition of bronchopulmonary dysplesia?

Answer 37

Infants who still have oxygen req at 36w post menstrual age.
Lung damage- from artificial ventilatiom- pressure/volume trauma, oxygen toxicity and infx.

CXR- widespread opacification -/+ cystic changes.

Tx- corticoisteroids- as lungs develop- facilitate earlier weaning from ventilators- however increase risk of cerebral episodes- so short courses.

A few- may die from- severe disease- intercurrent infx or pulmn HTN.

Question 38

What are some problems following preterms discharge?

Answer 38

Iron supplements to prevent anaemia till 6M. (Iron from solid foods)
Multivitamins.
Standardised immunisation.

Med probs- increased risk of:
Poor growth- VLBW- 90% 2-3 Y to catch up.
Pneumonia/wheezing/asthma.
Broncholitis from RSV( resp dyncytial virus) - hospitalisation reduced by the use of monovlonal Abs.
Chronic lung disease- may req additional oxygen therapy for many M
Gastro-oesophageal reflux- esp w/ bronchopulmonary dysplesia.
Complex nutritional and gastrointesrinal disorders- following necrotising enterocolitis or GI surgery
Inguinal hernias- req surgical repair.
Readmission- x4- resp and surg repair of hernias.

Monitor growth development- for learning- commonest- coordination, vision, hearing, cerebral palsy, behaviour, attention.
Deficits:
Fine motor skills- threading beads,
Conce- short attention span,
Behavioural probs- attention deficit disorder (kouvelis)
Abstract reasoning- mathematics
Processing several tasks simultaneously.

Question 39

Why do infants become jaundiced?

Answer 39

50% of them.
1. High Hb at birth- so physiological release of Hb from red cell brakdown
. Red cell lifespan newborns- 70days- adults- 120days.
2. Hepatic bilirubin metabolism less effiecient- ⬇️ bilirubin conjugation.

Neonatal jaundice imp:

1. Sign of another disease- hemoylitic anaemia, infx, metabolic disease, liver disease.
2. Unconjugated bilirubin(lipid sol) - can be deposited in brain( passes BBB-lipid soluble) , deposited in basal ganglia –> kernicterus.

Question 40

What happens in haemolysis?

Answer 40

1. Breakdown product of Hb-> unconjugated bilirubin. - insoluble in water but lipid soluble.
2. Carried in blood bound to albumin.
3. Albumin Bindining saturated, free unconjugated bilirubin passes through BBB as it is lipid soluble.
4. Unconjugated bilirubin taken up by liver and conjugated by enzyme:
   Glucuronyl transferase to conj bilirubin.
5. Thats water soluble and excreted in bile and into gut - strectobiloruninA faeces, urobilinogen- urea.
6. Detectable in urine when blood level rises.
7. Reabs of bilirubin from gut (enterohepatic circulation) is increased when milk intake is low.

Question 41

What does jaundice from

Answer 41

Thats its most propably from haemolysis.

Imp to identify as unconjugated bilirubin can rise rapidly and reach extreme high levels.

Question 42

What are some heamolytic disorders?

Answer 42

1.Rhesus haemolytic disease-
Identified Antenatally- tx at 28+34w- anti-D Abs.
Birth of severly affected- anaemia, hydrops, hepatosplenomegaly, rapidly developing severe jaundice, - rare cz we find it.
Antibodies developed to Kell or Duffy blood groups less severe.,

2. ABO incompatibility- more common
   Most ABO Abs- are IgM and do not cross placenta.
   Some group O women have IgG anti-A-hemolysin in blood which crosses the placenta and hemolyses Red cells of blood group A.
   Same w/ IgG-B-henolysin. Severe jaundece but less severe than rhesus. No hepatosplenomegaly.mpeaks im 12-72hrs.

Direct Abs test: Coombs test is +ve- demonstrates antibody on surface of red cells.

G6PD deficiency- Mediteranean, middle-east, far east or african americans. Mainly male infants.

Spherocytosis- less common than G6PD- fhx- spherocytesnidentifiednin blood film.

Question 43

What are some causes of jaundice at 2-14Days?

Answer 43

1.Physiological jaundice-
Bilirubin rises as adaptation to transition.
2.Breastfeed jaundice- hyperbilirubinaemia is unconjugated- increased enterohepatic bilirubin circulation.,
3.Dehydation- exacerbated if milk intake poor from feeding delay - dehydrated. IV fluids sometmes needed.
4. Infection-
Unconjugated hyperbilirubinaemia- poor fluid intake, healomysis, reduced hepatic fx + increase in enterohepatic circulation.
Esp UTI !
5. Other causes- bruising + polycythaemia (venous haematocrit is >0.65) exacerbates it.
6. Rare- Crigler-Najjar syndrome - enzyme glucuronyl tramsferase is deficient/abscent. –> ⬆️⬆️ extreme heights of unconjigated bilirubin–> persistent jaundice >2w, 3w in preterm.

Question 44

What are some causes of jaundice at >2w?

Answer 44

Unconjugated:
Physiological or breastfed- commonest-15% - fades by 4-5w
Infx- UTI
Hypothyroidism- jaundice before other sx- hypotonia, dry skin, coarse facies, constipation.
Haemolytic anaemia- G6PD deficiency
High GI obstruction- pyloric stenosis.

Conjigated: dark urine + unpigmentated pale stools. Heparomegaly and poor wt gain.
>25 mmol/L
- bile duct obstruction, biliary atresia,
Neonatal hepatitis.

Question 45

What should be avoided in severe jaundice and why?

Answer 45

Gestation:
Preterms and infants who experienced - lower threshold to treatment.
Clinical comdition:
severe hypoxia, hypothermia or anything serious- more susceptible to high levels of bilirubin- damage from severe jaundice.

Drugs which may displace bilirubin from albumin are avoided- sulphonamides, diazepam

Question 46

How would you manage neonate jaundice?

Answer 46

Poor milk intake and dehydration exacerbate it, so should be corrected.
1. Phototherapy- blue- green (450nm) light in visible spectrum converts unconjugaed bilirubin to a harmless water soluble pigment excreted in the urine. It’s eyes are covered- would dry.

2. Exchange transfusion- if bilirubin rises to potentially dangerous levels. Blood removed in small amounts- arterial line or umbilical vein- + replaced by donor blood.mtwice its blood volume is exchanged- 2x80ml/kg. risk of mortality.
   Donour blood- as fresh as possible, svreened for CMV, HIV, hep B and C.

Phototherapy reduced need for exchange. If ABO incompatibility- give immunoglobulins- reduce need for exchange.

Question 47

What are some causes of respiratoty distrss?

Answer 47

Common: transient tachypnoea of newborn
↪️ delay in resorption of lung liquid coomonest after birth on a C/S. CXR may show liquid. Diagnosis after exclusion. resolves within days.
Less common- meconium aspiration, pneumonia, RDS, persistent pulmonary HTN, milk aspiration, diaphragmatic hernia, tracheo-oesophageal fistula (TOF)
Pulmonary hypoplasia
Airway obstruction- choanal atresia
Pulm haemorrhage.

Non pumonary-
Congenital heart disease
Intracranial birth trauma/ encephalopathy
Severe anaemia
Metabolic acidosis

Question 48

What are the clinical Features of respiratory distress?

Answer 48

Tachypnoea>60breaths/min.
Labourwd breathing w/ chest wall rescession - esp syernal + subcostal indrawing + nasal flaring.
Expiratory grunting
Cyanosis if severe

Admitted NU- monitor- heart, resp rates, oxygenation + circulation.
CXR- identify cause , pneumothorax, / diaphrgmatic hernia.

Additional ambient oxygen , mechanical ventilation amd circulatory support.

Question 49

What happens in meconium aspiration?

Answer 49

Earliest srool- amniotic fluid, intreepithelial cells…
Increasingly Passed with increasing gestational age affecting 20-25% at 42w.
May be passed in response to fetal hypoxia.
At birth- may inhale thick meconium. Asphyxiated infants may start gasping and aspirate even more at delivery.

Its a lung irritant- mechanical obstruction amd chemical pmeumonitis- predisppsing to infx.

Lungs are over-inflated, + patches of collapse and consolidation.
High incidence of air leak –> pneumothorax, pneumomediastinum.

Artificial ventilation required.
May: persistent pulm HTN.

Severe- morbidity and mortality.

Question 50

What happens in pneumonia and pneumothoraces amd milk aspiration?

Answer 50

Pneumonia-
RFs- prolonged rupture of membranes, chorioamnionitis, +LBW predispose to pneumonia.
RDS infants - invx- broad-spec Antibiotics arebstarted early until results available- Narrow spec.

Pneumothorax- 2% spontaneous- asymptomatic or may cause RDS.
2o to meconium aspiration, RDS as a complication to ventilation.
Tension- drain

Milk aspiration-
More frequently- preterm infants , RDS, neurological damage.
Bronchopulmonary dysplesia- GORD- predisposed to aspiration.,
Infants w/ cleft palate- predispose to aspiration.

Question 51

What happens in persistent pulm HtN?

Answer 51

❌LIFE THREATENING❌ assc w/ birth asphyxia, meconium aspir, septicaemia, RDS. Sometimes 1o disorder. ⬆️ pulmonary vascular resistance : R–> L ahunting.
PDA( L->R)
Cyanosis soon after birth.
Heart murmurs + signs abscent CXR- heart normal size– SO URGENT
ECHO- no congenital heart disease.

Mech ventilation and circulatory support.
Inhaled NO-notric oxide- potent vasodilator.
Viagra- vasodialator.
ECMO- very severe- on heart and lung bypass- only special centres.

Question 52

What happens in diaphragmatic hernias?

Answer 52

Usually left side-
1 in 4000 births.
ANC USS.
CF-
Failure to respond to resuscitation,resp distress.
Left sided herniation of abdo contents through posterolateral foramen of diaphragm.
Apex and beat sounds displaced to right chest side. Poor air enrty on left chest.
Vigorous rescusutation–> may cause a pneumothorax in normal lung, therefore aggrevating the situation.

Dx- confirmed by CXR + AXR.
Tx- large NG tube is passed and suction applied to prevent distention of intrathoracic bowel
After stabilisation- hernia surgicly repaired.

Pulmonary hypoplesia - compression by herniated stuff throughout pregnancy has prevented normal development of lung–> death. Mortality high.

Question 53

What are some CF of neonate septicaemia?

Answer 53

Poor feeding
Fever- or temp instability or hypothermia.
Vomitting
Apnoea and bradycardia
Resp distress
Abdo distention
Jaundice
Neutropenia
Irritability
Seizures
Lethargy, drowsiness
Jandice

In meningitis:
Tense or bulging frontalle

Early onset infx-
FBC + blood cultures + 2 CRP (after 12-24hrs)
Tx- IV antibiotics gram +ve (amoxicillin) + cover gram -ve. (Aminoglycoside- gentamicin)
If cultures +ve, CSF culture to check for meningitis.

Late-onset infx-
Central venous catheters for parenteral nutrition, invading procedures that break barriers of skim and tracheal tubes.
Coagulase -ve stap epidermidis commonest.
Gram +ve- staph aureus, enteroccocus faecallis
Gram -ve: echeria coli, pseudomonas, klebsiella, serratia species.
Resistance or too preterm- vancomycin.

Use of prolonged broad spec antibiotics predisposes to fungal infx- candida albicans.

Tx- ambpicillin/ penicillin + rd gen cephalosporin - cefotaxime.

Question 54

What happens in group B strep?

Answer 54

10-30% of pregnant women- faecal or vaginal carriage.
Causes early and late onset sepsis.
Early- resp distress and pneumonia–> septicaemia and meningitis.
+ve blood or CSF culture- mortality 10%.
Late onset- 3M-
Meningitis, osteomyelitis or septic arthritis.

Rfs- preterm, prolonged rupture of membranes, maternal fever during labour >38degrees, maternal chroinamnionitis, or previously imfected infant.

Prophylaxis-
Intrapartum antibiotics IV to mum (during labour) can prevent transmission. Screening at 35-38 weeks to identify if infected( USA and Australia)

Question 55

Why is the injection done at intrapartum?why dont we screen for it?

Answer 55

Many might be allergic- allergic rctn might kill the baby.

So give it during labour- child not affected as much.

Question 56

What happens in Hep B babes?

Answer 56

If infant HBsAg (hep B surface antigen) +ve receive hep B vaccine shortly after birth.
Vaccination course continues during infancy and Abs checked.

When mum HBeAg +ve ( high infectivity) risk of infants becoming chronic carriers and have no HBeAg anti-E antibodies.
These ones should also be given passive immunisation with Hep B immunoglobulin within 24hrs.