Neonatal complications Flashcards
asphyxia
Oxygen deprivation. Failure of initiation of respiration in the newborn infant. Blood oxygen levels are low and the co2 is very high
causes of asphyxia
- Preterm birth
- Obstruction
- Certain drugs
- Congenital anomalies
- Cerebral damage
- Infection
- Haemorrhage
- Pneumothorax
- Pharyngeal suctioning
antenatal factors asphyxia
- Diabetes
- Pre-eclampsia
- Anemia
- Previous fetal death
- Maternal infection
- Polyhydramnios
- Oligohydramnios
- PROM/PPROM
- APH
- Post term
- Multiple gestation
- IUGR/SGA
- Drug abuse
- Congenital abnormalities
intrapartum factors asphyxia
- LSCS
- Malpresentation
- Premmie
- PROM
- Precipitous labour
- Prolonged labour >24 hrs
- Prolonged second stage > 2 hrs
- Non-reassuring FHR patterns
- Use of GA
- Narcotics administered within 4 hours of delivery
- Mec stained liquor
- Cord prolapse
- Placental abruption
- Placental previa
meconium aspiration syndrome
- Evident in around 10-15% of all labours but MAS only <1% of all live births
- More common in near-term or term babies
mechanism meconium aspiration syndrome
- Fetal hypoxia causes increased gut paralysis and relaxes the anal sphincter passage of meconium
- Fetal gasping occurs under stress meconium then becomes trapped in the airways allowing air in but not out
- Results in air accumulating behind the blockage which causes the alveoli to rupture (pneumothorax) pneumonitis as meconium touches the lung tissue
meconium aspiration syndrome treatment
- Babies need full NICU care and ventilation to minimise further deterioriation
- Oxygen therapy and antibiotics may be needed to avoid pneumonia
- Surfactant therapy commenced within 6 hrs of birth may reduce the severity of respiratory problems and may improve the prognosis
transient tachypnoea
- Commonly found in otherwise healthy, near term or full
- Mild surfactant deficiency or failure to absorb lung fluid
- LSCS, perinatal hypoxia – increased risk
transient tachypnoea signs and symptoms
- Tachypnoea – 60-120 breaths per min (rapid
- Nasal flaring
- Sternal recession
- Expiratory grunting
- Possible cyanosis (bluish-purple)
transient tachypnoea management
- Colour – pink
- Resp rate
- Good muscle tone
- Heart rate (check every 15 mins)
- Paed review
- Symptoms usually resolve within 24 hrs
- Important to rule out infection – chest x-ray, blood gases and cultures
- SCN admission – oxygen etc
respiratory distress syndrome
- Diagnosis of HMD is derived from the presence of hyaline membranes in the airways resulting from the damaged epithelium
- Condition seen in preterm infants caused by a lack of surfactant
- RDS – more neonatal deaths than any other condition and the incidence is inversely proportional to gestational age –
- 70% of neonates 29 weeks – rarely seen after 37 weeks
- X-ray across the lung fields
RDS management
- Correct diagnosis
- Exclude septicaemic pneumonia, antibiotics
- Blood cultures (detect bacteria and yeasts) and gases
- Surfactant therapy: administered directly into the bronchi in RDS within 15 mins of birth
- Oxygen therapy and ventilation
- Intermittent & continuous observations
apnoea
- Cessation of respiratory effort for 20 secs – constant monitoring
- Physiology: immature respiratory centre and immaturity of chemoreceptor response to hypoxia and acidosis
- First sign of sepsis, pneumonia, NEC or meningitis
chronic lung disease
- Preterm who requires supplemented oxygen supply at 36 weeks post conceptual age or beyond 28th day of life
- Risk factors
- Prematurity
- Endotracheal intubation
- High level ventilator PIP
- Oxygen toxicity
pneumothorax (air leak syndrome)
- Occurs when the alveoli rupture causing air to enter the pleural cavity
- Spont – at birth on initial inspiration or following mec aspiration, approx 1% of all newborns
- Induced – high ventilator settings, maldistribution of ventilated gas in the lungs
- Needle aspiration and underwater drain to resolve some serious cases
Congenital diaphdragmatic hernia
- 1: 2200-4000 live births
- Poor prognosis due to pulmonary hypertension and pulmonary hypoplasia
neonatal infections
multiple sources - skin, eyes, mouth and cord
TORCH viruses
toxoplasmosis
other viruses (parvovirus)
rubella
cytomegalovirus
herpes (varicella, listeriosis, hepatitis)
intrauterine infection
40% preterm
pathogenesis 4 ways
* Ascending infection from the lower genital tract
* Retrograde passage of organisms from the peritoneal cavity via the fallopian tubes
* From maternal circulation
* Invasive antenatal diagnostic procedures
intrauterine infection predisposing factors
- Transplacental infection
- Preterm birth
- Low birth weight
- Prolonged ROM
- Hypothermia
- Birth trauma
increased risks of intrauterine infection
membranes ruptured >18 hours
length of labour >12 hours
instrumental birth
VE
prevention intrauterine infection
- Inutero
- Hand hygiene
- Equipment
- Environment
- Invasive procedures
- Nosocomial
mild eye infection
- 1-2 days – chemical irritation
- Treat by wiping away secretions with cotton wool soaked sterile water
conjuctivitis
- Purulent discharge
- May be caused: Staphylococcus aureus, E.coli , Neisseria gonorrheae, Chlamydia trachomatis, Pseudomonas aeruginosa
- Treatment: clean eyes as above and 1 drop of chloramphenicol 1.0% 4 times a day for up to 5 days
Coagulase Negative Staphylococcus (CONS)
mortality higher in LBW babies and those babies who had undergone interventions. Prognosis worse if 3 or more sepsis screen parameters or clinical manifestations of sepsis are present
Omphalitis
infection of the periumbilical skin risks the spread via the umbilical vein, giving rise to thrombophlebitis and possibly leading to suppuration in the liver with severe jaundice. May result in portal hypertension with oesophageal varices in later childhood.
General skin sepsis
need to culture and treat. Minor lesions with antiseptic powder. Don’t overdo antibiotics as encourages MRSA. If needed flucloxacillin is a good first choice as most skin infections are caused by staphylococci
upper respiratory tract infections
- Snuffles – excess nasal secretion is common – blocks airways
- Respiratory syncytial virus: relatively mild URTI
- Acute bronchiolitis: seen in older infants and is severe
GIT infections
- Gastroenteritis or necrotising enterocolitis (NEC) NEC is inflammation of the gut wall as a result of infection. Recognised by acute abdominal pain, blood in the stools and vomiting, the condition may lead to septicaemia and be life threatening.
- Causative organisms (for gastro) include: – Rotavirus, Salmonella, Shigella, and a pathologic strain of E.coli * Secretory IgA in breast milk offers protection against these especially rotavirus. Priority is urgent correction of fluid and electrolyte imbalance
- Probiotic therapy for NICU babies
signs of neonatal infection
- Lethargy
- Vomiting
- Diarrhoea
- Jaundice
- Pyrexia
- Hypothermia
- Irritability
- Poor feeding
- Weak cry
- Abdominal distension
- Rashes
specific signs of infection
- Resp distress, bulging fontanelle
- Raised C-reactive protein
investigating
- FBC and blood gases
- Blood culture
- Urine or mec culture
- Swabs
- Lumbar puncture
- Chest x-ray, CT, MRI
- CRP
- Culture of amniotic fluid, placental tissue and cord blood
causative organisms
- Early onset – (first few days) GBS, E.coli, L.monocytogenes (blood borne from GIT infections)
- Late onset – over half caused by coagulase negative Staphylococcimany of which are resistant to Methicillin
- Treatment
- IV Antibiotics will commence prior to ID of causative organism
- Combination of Ampicillin & Gentamicin or Cefotaxime
- Drugs may change when causative organism is identified and according to the pattern of infections seen in each neonatal unit
GBS
10% of babies
- Early (within 12 hours of birth) or late (usually at 4-5 weeks)
- Ongoing controversy regarding screening of GBS in pregnancy: Incidence of asymptomatic vaginal GBS carriers = 12-15%
- May be subtle and nonspecific, within hours the baby can rapidly deteriorate
- Acute septicaemic infection with the signs of respiratory distress – Local signs are generally confined to fine rales on auscultation
- A chest X-ray is essential for differentiating infection from the many other causes of respiratory distress
midwifery care infections
- Antenatal history
- Promote general nutrition
- Labour and birth history
- Attend to obs
- Refer when indicated
- Eye washes
- B/F
- Education
- Documentation
jaundice
- Fetal liver
- Prominent by 7 weeks gestation – 9-12 weeks erythropoiesis decreases in the liver and begins in spleen – Reaches metabolic maturity relatively late in gestation, storing glycogen in the last 9 weeks – Bile production
- Inutero the placenta removes the bilirubin from the fetus so that it can be processed by the mother’s liver
- At birth the baby’s liver initiates that role
Physiology of bilirubin metabolism
- When RBCs age, are immature or malformed they are removed from the circulation and broken down in the reticuloendothelial system (liver, spleen and macrophages)
- haem which is converted to unconjugated bilirubin. – globin which is broken down into amino acids and then used by the body to make proteins. – iron which in turn is either stored by the body or recycled to make new blood cells
2 forms of jaundice - Unconjugated bilirubin
indirect bilirubin
– Cannot be easily excreted from the body by urine or bile as it is fat soluble. – Is deposited in the connective tissue of the skin, with excess levels = yellow skin colour.
– Is transported to the liver, linked/bound to albumin for processing.
– Being fat soluble has the potential to cross the blood brain barrier to cause bilirubin staining and toxicity known as kernicterus.
2 forms of jaundice - conjugated jaundice
= direct bilirubin
- Has been processed by the liver to become water soluble, and then can be easily excreted from the body, mainly through faeces and urine.
- Some conjugated bilirubin is hydrolysed back to unconjugated bilirubin in the colon. This unconjugated bilirubin is then absorbed across the intestinal mucosa into the capillaries.
what is jaundice
- Yellow discolouration of the skin
- Common
- Early neonatal jaundice is usually caused by the physiological destruction of red blood cells in the infant, and its importance lies in the ability of the bilirubin pigment to cross the blood brain barrier resulting in neurotoxicity
what causes jaundice
- due to an immature liver system and not effectively coping with RBC destruction and the decreased hepatic blood flow.
- During the first 3-4 months following birth, destruction of RBCs exceeds production.
- Neonatal RBCs have a shorter lifespan than adult RBC, and preterms even shorter.
- What babies are at risk? – 60% of term babies and 85% preterm babies develop jaundice in the first week of life NSW Health Agency for Clinical Innovation – About 10% breast fed babies are still jaundiced at age 1 month.
physiological causes jaundice
- Gestational age
- Delivery
- Hypoxia
- Hypothermia
- Hypoglycemia
- Poor feeding
- Urinary infection
pathological
- Abo incompatibility
- Weak postivie to direct coombs test
- Resulting jaundice usually treated with phototherapy
- Rarely requires exchange transfusions
rhesus incompatibility
- Mum Rh negative and produces antibodies against an Rh positive baby who has inherited the dominant Rh positive gene from the Dad
- More an issue in subsequent pregnancies when antibodies are pre-formed
