Neonatal Flashcards
Prematurity defintion
Under 37 weeks gestation
Potential premature rupture of membranes - managenet
Refer to midwife/obstetrics
- USS to check baby; is she going into labour;
- Erythromycin for 10 days to reduce risk of chorioamnionitis + can delay labour
- Give STEROIDS if after 22 weeks (improves baby’s underdevelopment - stimulates surfactent production)
- no point if <22 weeks
What makes a fetus at higher risk from prematurity
Male
Fetal grwoth restriction
Multiple preg
No Anternatal steroids
Steroid course to improve prematurity outcome
12 mg betamethasone, 24 hours apart, hopefully up to 24 hours before delivery
What assements to do for fetus in premature rupture of membranes
Fetal blood flow using Doppler
- absent end diastolic flow (poor outcome)
- reversed end diastolic flow (iminent death)
Mainstays of fetal wellbeing
- Is fetus moving
- Fetal size (size of bump in cm)
- Does baby have heartbeat
probability of premature survival rate
23 ~30%
25 weeks ~70%
28 weeks ~90%
Managment for fetus at high risk of demise
- A few weeks of STEROIDS
- IV MgSO4 (neuroprotection - reduces risk of cerebral palsey if given within 24 hours of birth)
- Consider delivering prem
When is surfactant released from type 2 pneumocytes
After 24 weeks
- lowers surface tension so alveoli don’t collapse
Ie RISK of RDS if born <28 weeks
Chronic lung disease of prematurity lung outcome
Hyperexpanded, diffusion defect, cystic changes
- alveoli don’t grow as much after prem birth
- caused by treatments for RDS
When is brainstem fully myelinated
32 - 34 weeks
Prems forget to breath occasionally (oft associated with bradycardia) because not fully myelinated
Apnoea of prem Tx
- NCPAP and Tactile STIMULATION
- PHOSPHODIESTERASE INHIBITORS ie IV CAFFINE (upregulates cAMP)
Neonatal haemorrhage
- Most commonly occurs in GERMINAL MATRIX (above caudate
nucleus) - Then VENTRICULAR (typically ok if only small amount of blood but has potential for huge amounts of blood to fill the space -> hypovolemic shock or hydrocephalus)
- Parenchymal
- CYSTIC PARIVENTRICULAR LEUKOMALACIA (can’t remodle - typically affects leg motor function but can get a full hemiplegia or even quadreplegia)
Infant benefit of breast milk
Less Infection:
Diarrhoea, Otitis media, Respiratory Syncytical Virus, Respiratory Infections, Enhanced Vaccine Response
Less immune driven/allergic disease:
Wheezing, Childhood cancer, Eczema, Hodgkin’s disease, Multiple sclerosis, Crohn’s disease, Diabetes mellitus, Enhanced immunologic development
Reduces risk of NEC
Reduced Reduced SIDS
Reduced Gastroesophageal Reflux
Lower risk of Childhood Inguinal Hernia
Higher IQ
Better Cognitive Development
Maternal benefits of breast feeding
Reduces cancer risk for:
Breast, Uterine, Ovarian, Endometrial
Improved health with less:
Post partum haemorrhage, postnatal depression, Decrease insulin requirements in diabetics, Osteoporosis later in life, Less child abuse
Promotes postpartum weight loss
Optimum child spacing
Less food expense
Less medical expense
More ecological
Delays fertility
Feeding prems
- Nasogastric tube for expressed milk
- PO from a cup once they can swallow
Doesn’t get suckling reflex till 32-34 weeks
Causes of Jaundice in neonates
Unconjugated: high levels cause kernicterus
Caused by: haemolysis, prematurity, sepsis, dehydration, hypothyroid, metabolic disease
High levels treated by phototherapy (blue light, 450 nm) or exchange transfusions
Conjugated: high levels not a worry
Caused by: prolonged parenteral nutrition, NEC, sepsis, metabolic, anatomical problems
When must jaundice be investigated in neonates
If lasting more than 3 weeks
(can leave for 5 weeks if prem as common for prem jaundice)
When does IgG transfer from mum occur
Last 3 months of gestation (prems get less of this + less active cell mediated immunity)
Necrotising enterocolitis
Bacterial invasion + large bowel ischaemia -> mural oedema + intramural gas -> can get perforation
Retinopathy of prem
- Hyperoxic insult (esp from O2 therapy)
- Arrest of normal vascular growth
- Fibrous ridge forms
- Vascular proliferation
- Retinal haemorrhages
- Retinal detachment
- Blindness
If high risk -> laser therapy
Parental help for prems/neonatal complications
Antenatal counselling
Post delivery counselling
Prognostic counselling
Regular updates
Palliative care counselling
Bereavement counselling
Meconium aspiration syndrome
- Triggered by passage of meconium into fetal lungs leading to blockage + inflam of airways
- significant risk of morbidity / mortality - Oft an indication of FETAL DISTRESS + HYPOXIA as these trigger intestinal / anal sphincter relaxation
- prematurly empties bowels into amniotic fluid
- could also just be because the baby is over-term
Meconium Ileus
Thickening of meconium -> obstruction
- commonly early indicator of cystic fibrosis
Meconium Aspiration Syndrome causes what in the neonate?
Initially seen through meconium in amniotic fluid (meconium stained liquor)
- Partial / Total Airway Obs
- potential lung collapse / air trapping
- SHUNTING + V/Q mismatch - Foetal Hypoxia
- Pulm inflam
- Infection
- increased risk of chemical pneumonitis -
Surfactant Inactivation
- due to inflam reaction caused by meconium -> more hypoxia -
Persistent Pulmonary Hypertension (PPHN)
- pulm vascular bed REMODELS due to hypoxia, vasoactive mediators + V/Q mismatch
Meconium ileus Sx
- Not passing meconium within 1st 24hrs of birth (max 48hrs)
- bilious vomiting
- distended abdo
Meconium Aspiration syndrome Ix
- Assess for meconium stained liquor
- CXR to evaluate lungs:
- INCREASED lung VOLUME
- Asymmetrical patchy pleural opacities
- Pleural EFFUSION
- Pneumo -thorax / - mediastinum
- Multifocal consolidation IF chemical pneumonitis - Bloods:
- FBC; CRP; Cultures
Consider:
- ABG
- Dual pulse oximetry
- Echo
- Cranial US
Meconium ileus
- Clinical exam
- Abdo X-ray / USS to confirm
- SWEAT TEST for CF
Meconium Aspiration Syndrome Mx
Observation + routine care:
- esp keep warm as hypothermia inhib surfactant production
- Potentially :
- O2 monitoring +/- THERAPY +/- Ventilation
- Abx to prevent 2ndry infection
- Surfactant bolus
- Inhaled Nitric Oxide if PULM HTN
Meconium ileus Mx
- Surgery
- Supplemental neutrition
- Mx CF if needed
Pathophys of meconium aspiration syndrome
- Foetal hypoxic stress / VAGAL STIMULATION due to CORD COMPRESSION causes PERISTALSIS
- once aspirated - stimulates release of:
- VASOACTIVE + CYTOKINES -> activates INFLAM pathways
- INHIBITS effects of SURFACTANT
The way it presents will vary depending on composition of meconium + neonate’s health e.g. foetal hypoxia + airway obstruction
RFx for meconium aspiration
- Gestational age > 42 wks
- Foetal distress (tachy/bradycardia)
- Intrapartum HYPOXIA 2ndry to PLACENTAL INSUFFICIENCY
- Thick meconium
- Apgar score <7
- Chorioaminonitis +/- Prolonged pre-rupture
- Oligohydroamniosis
- In utero GROWH RESTRICTION
- Maternal conditions:
- HTN, diabetes, pre/eclampsia, smoking, drugs
APGAR score
- Appearance
- (0 = cyanotic/pale all over; 1 = periph cyanosis) - Pulse
- (0= no pulse; 1= <100) - Grimace (reflex irritability)
- (0= no response to stimulation; 1 = only weak response) - Activity (tone)
- (0 = floppy; 1 = some flexion) - Respiration
- (0 = apneic; 1 = slow, irregular breathing)
Should be getting 2 points on all
Taken 1 minute after birth + 5 min after birth
Normal APGAR score
7-10
< 7 = re-evaluation; <4 = BAD
Meconium aspiration syndrome Px
Signs of resp distress:
- Tachypnoea – a respiratory rate of >60 breaths per minute
- Tachycardia – a heart rate of >160 beats per minute
- Cyanosis – this requires immediate management
- Grunting
- Nasal flaring
- Recessions – intercostal, supraclavicular, tracheal tug
- Hypotension – systolic blood pressure of <70 mmHg
Complications of meconioum aspiration
- Air leak due to “ball-valve effect” -> pneumothorax
- Persistant pulmonary HTN
- Cerebral palsey due to hypoxia
- Chronic Lung disease
- due to barotrauma + O2 TOXICITY
RFx for necrotising enterocolitis
- V low birth weight / prematuritiy
- Intrauterine growth restriction
- Formula feeding
- Resp distress + assisted ventilation
- Hypoxia - Sepsis
- Patent ductus arteriosus / other cong heart abnormalities (also causes hypoxia)
- Polycythemia
- Exchange transfusion
Necrotising enterocolitis Px
- Feeding intolerance
- Vomiting (esp if green bile)
- Haematochezia
- Distended, tender abdomen
- Absent bowel sounds
- Generally unwell
Will go into shock if peritonitic
Necrotising enterocolitis Ix
Bloods:
- FBC, U+E (hyponatraemia)
- CRP
- Cultures
- Capilarry blood gas (metabolic acidosis)
X-ray (diagnostic):
- Dilated bowel loopsa
- Thickened bowel walls (oedema)
- Pneumatosis intestinalis (gas in bowel walls)
- Pneumoperitoneum (perforation)
- Gas in portal veins
Necrotising enterocolitis Mx
Medical for 10-14 days (if stage 1/2)
- NIL BY MOUTH
- IV fluids, total PARENTERAL neutrition + ANTIBIOTICS
- NG tube can be used to drain fluid + gas from stomach / intestine
- any supportive Tx e.g. correct Acid-base; ventilation
Surgical emergancy if:
- Intestinal PERFORATION
- GI OBS due to stricture formation
- Deterioration despite medical Mx
IMMEDIATE REFERRAL to neonatal surgical team
- mc = intestinal resection with stoma formation
Necrotising enterocolitis staging
Bell scoring system
- Suspected NEC - bowel distension only on x-ray
- lethargic
- unstable temperature
- apnoea + bradycardia
- Vomiting
- Blood in poo
- Abdo distend - Definite NEC - Bowel distension, Portal venous gas + PNEUMATOSIS INTESTINALIS
- All the general stuff + metabolic acidosis + thrombocytopenia
- Can get absent bowel signs + tenderness - Advanced NEC - All of above + Pneumoperitoneum (PERFORATION)
- marked GI BLEEDING + systemic abnormalities
- can get DIC
Complications of Necrotising enterocolitis
- Perforation, sepsis + death
- Absecess formation
- Long term
- intestinal stricture
- Short bowel syndrome
- Long term stoma
Can recur
Gastroschisis meaning
Birth defect where there is a hole in abdo wall allowing intestines + sometimes other organs to herniate out
- no covering membrane
Omphalocele meaning
Abdo organs protrude out through hole in belly - covered by thin sac (formed by amniotic membrane + peritoneim)
Mx for gastroschisis
Can attempt vaginal delivery but Newborn should go to theatre as soon as possible (within a few hours)
Omphalocele Mx
- C-section to reduce risk of sac rupture
- Consider a staged repair as primary closure can be difficult due to lack of space / high intra-abdo pressure
- Sac is allowed to granulate + epithelialise (over wks/months)
- As infant grows the sac contents will eventually be able to fit into abdo cavity so shell is removed + abdomen closed
oesophageal atresia
upper + lower oesophagus don’t connect
- oft associated with tracheoesophageal fistula + other congenital defects
Px with unable to feed + sometimes breathing difficulties
Diff types of oesophageal atresia
- Type A - both upper + lower oesophagus = blind ended tubes
- Type B (rare) - upper part attached to trachea + lower part has closed end
- Type C (mc) - lower part connected to trachea + upper part blind ended
- Type D (rarest + most severe) - both parts of oesophagus connected to trachea (means food passes through trachea)
Oesophageal atresia Dx
Usually found when baby chokes / vomits when trying to feed or when NG tube insertion attempted
- confirm with X-RAY
Tx of oesophageal atresia
Surgery
Complications:
- Stenosis
- Muscles too weak to pass food to stomach
- Food keeps getting regurgitated into oesophagus (weak LOS)
Bowel atresia
Bowel is completely blind ended - Tx with surgery
Small bowel atresia more common than duodenal atresia
Colonic atresia is very rare
Px of bowel atresia
Same as intestinal obstruction
- Difficulty feeding
- Abdo distension
- Vomiting (bilious usually)
- No flatulence
- No passage of meconium / only small amount (tho sometimes this is normal)
- May have jaundice
Bowel atresia Dx
- May be able to see POLYHYDRAMNIOSIS on USS antenaltally
- Clinical Px after birth + X-RAY showing obstruction
- may do a contrast scan / enema as well as / instead of X-ray
- Laproscopic investigation sometimes to decide if laperotomy is needed
Bowel atresia Mx
- Nil by mouth + IV fluids + total parenteral nutrition
- NG tube to remove gas + fluid
- Surgery
- Anastemosis (can sometimes leak - Tx with Abx)
- Stoma
- Sometimes there will be further atresia (checked during surgery but not always picked up)
Cleft lip / cleft palate
- Cleft lip = split/open section of upper lip which can extend up to nose
- Cleft palate = defect in hard OR soft palate - opening between mouth + nasal cavity
Can occur together or on their own
Usually occcurs randomly but slightly higher risk if close relative also had
Complications caused by cleft lip / palate
PRoblems with feeding, swallowing + speech
Not life-threatening but significant PSYCHO-SOCIAL implications - including bonding between mum + baby
Can be more prone to - hearing problems, ear infections + glue ear
Cleft lip / palate Mx
Specialist cleft lip services MDT
- plastics, maxillofacial + ENT surgeons; dentists; specialist nurses; SALT; psychologists; GP
- specially shaped bottles / teats to ensure baby can feed
- Surgery
- for cleft lip at 3 months
- for cleft palate at 6-12 months
- specialist nurse follow up through surgery + beyond to ensure good development
RFx for gastroschisis
- Younger maternal age (more common in teen mums)
- Alcohol + tobacco
- Genitourinary infection within 3 months of becoming preg
What are the 2 categories of neonatal sepsis
- Early onset (within 72 hrs of life)
- Notably things like Strep B, Listeria, Toxoplasma, Rubella, CMV (TORCH infections baso - get from mother)
- Late onset (after 72 hrs)
- Predominantly from Staph aureus, staph epidermidids, E coli, Pseudomonas + Klebsiella (hospital acquired or from GI tract)
Both have to occur in infants < 90 days to be classed as Neonatal
Which pathogens causing early onset neonatal sepsis ascend from cervix + Tx
- Ecoli
- Strep B (mc)
Typically presents as asymp bacteriuria / UTI in mum and there is no routine testing for strep B
Tx with IV BENZYLPENICILLIN during childbirth if shows RFx
Transplacental causes of early onset neontal sepsis
- Listeria
- Toxoplasma
- Rubella
- CMV
RFx for early onset neonatal sepsis
- Multiple preg with a sibling who has suspected/confirmed infection
- Evidence of GBS in any preg
- PREMMIES
- Rupture of membranes for:
- >18 hrs for premmies
- >24 hrs for term babies - Maternal intrapartum temp >38 C
- Suspected/confirmed Maternal SEPSIS
- CHORIOAMNIONITIS
NB - bold = RED FLAG
Clinical indicators suggesting early onset neonatal sepsis (name at least 5)
- Altered behaviour / responsivesness
- Altered muscle tone
- Feeding difficulties
- feed intolereance e.g. Vomiting, excessive gastric aspirates + Abdo distension
- Abnormal heart rate
- Resp distress
- Apnoea
- Hypoxia
- Jaundice
- Signs of neonatal encephalopathy
- Need for CPR
- Need for mechanical ventilation in premmie
- Persistent fetal HTN
- Abnormal temp
- Abnormal cogulation / bleeding
- Oliguria for >24hrs post birth
- Altered glucose levels
- Metabolic acidosis
- Local signs of infection
Red flags suggestive of early onset neonatal infection
- Systemic Abx given to mother for suspected bacterial infection within 24hrs of birth
- SEIZURES
- Signs of SHOCK
- Respiratory distress starting > 4 hours after birth
- Need for mechanical ventilation in TERM baby
- Suspected / confirmed infection in a sibling in a multiple pregnancy
Neonatal sepsis Ix
- FBC, CRP + Blood cultures (1st before atarting Abx)
- CRP must be repeated by 24-36 hrs after initial Abx dose - Swabs / cultures if an obvious source
- tho urine cultures not advised (difficult to obtain + not super reliable)
- LP if strong clinical suspicion + safe to do so
- also can consider if 1st 2 CRP raised; blood culture +ve; baby doesn’t respond to Abx - CXR if strong suspicion of chest source
Tx for neonatal sepsis
- IV BENZYLPENICILLIN + GENTAMICIN (empirical)
- consider stopping after 36 hrs if:
- blood cultures -ve; initial clinical suspicion not strong; clinical condition of baby reassuring; levels of CRP good
- consider stopping after 36 hrs if:
If blood cultures +ve
-> ABX CONTINUE for 7 - 10 DAYS (up to 14 days if CSF +ve)
- if -ve but CRP raised - consider Abx for 5 DAYS
Must monitor gentamicin as it can be toxic
Congenital rubella syndrome aet
Caused by maternal rubella infection during first 20 WEEKS of preg (esp in first 10 WEEKS)
Prevention of congenital rubella syndrome
- MMR vaccination for mother before pregnancy (2 doses - 3 months apart)
- test for rubella immunity if in doubt
DO NOT GIVE IF ALREADY PREG - IT IS A LIVE VACCINE!
- wait till postpartum!
Congenital Neonatal Rubella (CRS) Px
- Sensorineural Deafnesss
- Cataracts / Retinopathy
- Cong. Heart disease (PDA, pulm stenosis)
Also:
- Organ dysfunction
- Microcephaly
- Micrognathia (small mandible)
- Low birth weight
- “BLUEBERRY MUFFIN” RASH (petechial)
- Haem abnormalities
- Learning disability
Ix of congenital rubella
Dx with SEROLOGY for rubella
- Audiology
- Opthalmology
- Echcardiography
CRS Mx
Supportive + symptomatic
- earlier the better
Regular follow-up to monitor
Congenital varicella syndrome Px
- Fetal growth restriction
- Microcephaly,
- hydrocephalus
- Learning disability
- Scars + significant skin changes in SPECIFIC dermatomes
- Limb hypoplasia
- Cataracts / Choriortinitis
Congenital varicella syndrome cause (ie what time period)
Maternal chickenpox in FIRST 28 WKS of gestation
Can Tx with oral aciclovir if >20 wks + Px within 24 hours of Sx starting
Lesteriosis epid
MORE LIKELY in preg women
can be asymp, flu-like or occasionally cause a pneumonia or meningoencephalitis
-> Miscarriage, fetal death or severe neonatal sepsis
Congenital CMV Px
- Fetal growth restriction
- Microcephaly
- Hearing loss
- Vision loss
- Learning disability
- Seizures
How is CMV usually spread
Via infected saliva / urine of asymp children
- usually CMV in preg doesn’t cause congenital CMV
Congenital toxoplasmosis Px
Classic Triad:
- Intracranial calcification
- Hydrocephalus
- Chorioretinitis
HIgher risk if caught later in preg
Complications of parvovirus B19 in preg
- Miscarriage / fetal death
- Severe fetal anaemia
- HYDROPS FETALIS (fetal heart failure)
- Maternal pre-eclampsia-like syndrome
esp if caught in 1st / 2nd trimesters
How does maternal parvovirus B19 infection cause fetal anaemia
- parvovirus infection ERYTHROID PROGENITOR CELLS in fetal bone marrow + liver
- faulty RBCs with shorter life span made
- Anaemia then leads to HF -> HYDROPS FETALIS
Maternal pre-eclampsia-like syndrome
AKA mirror syndrome
Severe hydrops fetalis causes placental oedema -> Maternal oedea, HTN + proteinuria
Need to check maternal IgM, IgG parvovirus Ab + Rubella Ab (DDx) if parvovirus is even suspected
