Neonatal medicine (1) Flashcards
1
Q
How are neonatel units organised?
A
- special care (level 1)
- short-term intensive care (level 2)
- long-term intensive care (level 3), usually linked to specialist fetal and obstetric care to form a specialist tertiary perinatal centre
2
Q
Hypoxic-ischaemic encephalopathy
A
- In perinatal asphyxia, gas exchange, either placental or pulmonary, is compromised or ceases altogether, resulting in cardiorespiratory depression
- Hypoxia, hypercarbia and metabolic acidosis follow
- Compromised cardiac output diminishes tissue perfusion, causing hypoxic-ischaemic injury to the brain and other organs
3
Q
Hypoxic-ischaemic encephalopathy
Causes?
A
(HIE) follows a significant hypoxic event immediately before or during labour or delivery:
- Failure of gas exchange across the placenta – excessive or prolonged uterine contractions, placental abruption, ruptured uterus
- Interruption of umbilical blood flow – cord compression including shoulder dystocia, cord prolapse
- Inadequate maternal placental perfusion, maternal hypotension or hypertension – often with intrauterine growth restriction
- Compromised fetus – anemia, intrauterine growth restriction
- Failure of cardiorespiratory adaptation at birth – failure to breathe.
4
Q
Hypoxic-ischaemic encephalopathy
Management
A
Skilled resuscitation and stabilisation of sick infants will minimise neuronal damage. Infants with HIE may need:
- respiratory support
- recording of amplitude-integrated electroencephalogram (aEEG, cerebral function monitor) to detect abnormal background activity to confirm early encephalopathy or identify seizures
- treatment of clinical seizures with anticonvulsants
- fluid restriction because of transient renal impairment
- treatment of hypotension by volume and inotrope support
- monitoring and treatment of hypoglycaemia and electrolyte imbalance, especially hypocalcaemia.
5
Q
Birth injuries (1)
Soft tissue injuries
A
- Caput succedaneum – bruising and oedema of the presenting part extending beyond the margins of the skull bones; resolves in a few days
- Cephalhaematoma – haematoma from bleeding below the periosteum, confined within the margins of the skull sutures. It usually involves the parietal bone. The centre of the haematoma feels soft. It resolves over several weeks
- Chignon – oedema and bruising from Ventouse delivery
- Bruising to the face after a face presentation and to the genitalia and buttocks after breech delivery. Preterm infants bruise readily from even mild trauma
- Abrasions to the skin from scalp electrodes applied during labour or from accidental scalpel incision at Caesarean section
- Forceps marks to face from pressure of blades – transient
- Subaponeurotic haemorrhage (very uncommon) – diffuse, boggy swelling of scalp on examination, blood loss may be severe and lead to hypovolaemic shock and coagulopathy
6
Q
Birth injuries (2)
Nerve palsies
Fractures
A
- Brachial nerve palsy results from traction to the brachial plexus nerve roots. Occur at breech deliveries or with shoulder dystocia. Upper nerve root (C5 and C6) injury results in an Erb palsy
- It may be accompanied by phrenic nerve palsy causing an elevated diaphragm
- A facial nerve palsy may result from compression of the facial nerve against the mother’s ischial spine
Fractures:
- Clavicle - Usually from shoulder dystocia. A snap may be heard at delivery or the infant may have reduced arm movement on the affected side
- Humerus/femur - Usually mid-shaft, occurring at breech deliveries, or fracture of the humerus at shoulder dystocia
7
Q
Jaundice (1)
A
Over 50% of all newborn infants become visibly jaundiced. This is because:
- there is marked physiological release of haemoglobin from the breakdown of red cells because of the high Hb concentration at birth
- the red cell life span of newborn infants (70 days) is markedly shorter than that of adults (120 days)
- hepatic bilirubin metabolism is less efficient in the first few days of life.
Neonatal jaundice is important as:
- it may be a sign of another disorder, e.g. haemolytic anaemia, infection, metabolic disease, liver disease.
- unconjugated bilirubin can be deposited in the brain, particularly in the basal ganglia, causing kernicterus.
8
Q
Jaundice (2)
Kernicterus
A
- encephalopathy resulting from the deposition of unconjugated bilirubin in the basal ganglia and brainstem nuclei
- occur when the level of unconjugated bilirubin exceeds the albumin-binding capacity of bilirubin of the blood
- free bilirubin is fat-soluble, it can cross the blood–brain barrier. The neurotoxic effects vary in severity from transient disturbance to severe damage and death
- manifestations are lethargy and poor feeding. In severe cases, there is irritability, increased muscle tone causing the baby to lie with an arched back (opisthotonos), seizures and coma
- used to be an important cause of brain damage in infants with severe rhesus haemolytic disease, but has become rare since the introduction of prophylactic anti-D immunoglobulin for rhesus-negative mothers
9
Q
Haemolytic disorders
Rhesus haemolytic disease
A
- Affected infants are usually identified antenatally and monitored and treated if necessary
- a severely affected infant, with anaemia, hydrops and hepatosplenomegaly with rapidly developing severe jaundice, has become rare
- Antibodies may develop to rhesus antigens other than D and to the Kell and Duffy blood groups, but haemolysis is usually less severe.
10
Q
Haemolytic disorders
ABO incompatibility
A
- More common than rhesus haemolytic disease.
- Most ABO antibodies are IgM and do not cross the placenta, but some group O women have an IgG anti-A-haemolysin in the blood which can cross the placenta and haemolyse the red cells of a group A infant.
- Occasionally, group B infants are affected by anti-B haemolysins.
- Haemolysis can cause severe jaundice but it is usually less severe than in rhesus disease.
- The infant’s haemoglobin level is usually normal or only slightly reduced and, in contrast to rhesus disease, hepatosplenomegaly is absent.
- The direct antibody test (Coombs’ test), which demonstrates antibody on the surface of red cells, is positive.
- The jaundice usually peaks in the first 12–72 h.
11
Q
Haemolytic disorders
G6PD deficiency
A
- Mainly in people originating in the Mediterranean, Middle-East and Far East or in African-Americans. Mainly affects male infants , but some females develop significant jaundice.
- Parents of affected infants should be given a list of drugs to be avoided, as they may precipitate haemolysis.
12
Q
Haemolytic disorders
Spherocytosis
A
- This is considerably less common than G6PD deficiency.
- There is often, but not always, a family history. The disorder can be identified by recognising spherocytes on the blood film.
13
Q
Jaundice at 2 days to 2 weeks of age
A
- Physiological jaundice
- Breast milk jaundice. Jaundice common in breast fed infants. Hyperbilirubinaemia is unconjugated.
- The cause is multifactorial but may involve increased enterohepatic circulation of bilirubin
- Dehydration
- Infection
14
Q
Management of Jaundice
A
- Poor milk intake and dehydration will exacerbate jaundice and should be corrected
- Phototherapy is the most widely used therapy, with exchange transfusion for severe cases
Exchange transfusion:
- Exchange transfusion is required if the bilirubin rises to levels which are considered potentially dangerous.
- Blood is removed from the baby in small aliquots, (usually from an arterial line or the umbilical vein) and replaced with donor blood (via peripheral or umbilical vein)
15
Q
Respiratory distress in term infants
A
- tachypnoea (>60 breaths/min)
- laboured breathing, with chest wall recession (particularly sternal and subcostal indrawing) and nasal flaring
- expiratory grunting
- cyanosis if severe
16
Q
Transient tachypnoea of the newborn
A
- Commonest cause of respiratory distress in term infants.
- delay in the resorption of lung liquid and is more common after birth by Caesarean section.
- chest X-ray may show fluid in the horizontal fissure.
- Additional ambient oxygen may be required.
- settles within the first day of life but can take several days to resolve completely.
- This is a diagnosis made after consideration and exclusion of other causes
17
Q
Other causes of RDS
A
- Meconium aspiration
- Pneumonia
- Pneumathorax
- Milk aspiration
- Persistent pul;monary aspiration
- Diaphrgmatic hernis
18
Q
Early-onset infection
A
- In early-onset sepsis (<48 h after birth), bacteria have ascended from the birth canal and invaded the amniotic fluid.
- The fetus is secondarily infected because the fetal lungs are in direct contact with infected amniotic fluid.
- These infants have pneumonia and secondary bacteraemia/septicaemia.
- In contrast, congenital viral infections and early-onset infection with Listeria monocytogenes, fetal infection is acquired via the placenta following maternal infection.
19
Q
Late-onset infection
A
- In late-onset infection (>48 h after birth), the source of infection is often the infant’s environment
- Nosocomially acquired infections are an inherent risk in a neonatal unit, and all staff must adhere strictly to effective hand hygiene measures to prevent cross-infection
- Coagulase-negative staphylococcus (Staphylococcus epidermidis) is the most common pathogen, but the range of organisms is broad, and includes Gram-positive bacteria (Staphylococcus aureus and Enterococcus faecalis) and Gram-negative bacteria (Escherichia coli and Pseudomonas, Klebsiella and Serratia species)
21
Q
Conjunctivitis
A
- Sticky eyes common in the neonatal period, starting on the 3rd or 4th day of life. Cleaning with saline or water is all that is required and resolves spontaneously
- more troublesome discharge with redness of the eye may be due to staphylococcal or streptococcal infection and can be treated with a topical antibiotic eye ointment, e.g. neomycin
-
Chlamydia trachomatis eye infection usually presents with a purulent discharge, together with swelling of the eyelids. Treatment is with oral erythromycin for 2 weeks
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22
Q
Herpes simplex virus (HSV) infections
A
23
Q
Hepatitis B
A
- Infants of mothers who are hepatitis B surface antigen (HBsAg)-positive should receive hepatitis B vaccination shortly after birth to prevent vertical transmission.
- The vaccination course needs to be completed during infancy and antibody response checked. Babies are at highest risk of becoming chronic carriers when their mothers are ‘e’ antigen-positive but have no ‘e’ antibodies.
- Infants of ‘e’ antigen-positive mothers should also be given passive immunisation with hepatitis B immunoglobulin within 24 h of birth.
Infants of HBsAg-positive mothers should be vaccinated against hepatitis B.
