Oxford Handbook of Midwifery (127 page)

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Authors: Janet Medforth,Sue Battersby,Maggie Evans,Beverley Marsh,Angela Walker

BOOK: Oxford Handbook of Midwifery
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  • GBS: the most common.
  • Herpes simplex: acquired through contact with genital secretions.
  • Hepatitis B: acquired through contact with vaginal secretions.
  • HIV: attributed to contact with infected secretions.
    Sexually transmitted diseases
    are on the increase in the UK and are transmitted during vaginal delivery. These include:
  • Chlamydiosis
  • Syphilis
  • Gonorrhoea—in the newborn this can cause conjunctivitis, which can develop into pneumonia.
    1
    ,
    2
    3 All healthcare workers are strongly advised to use universal precau- tions routinely when in contact with maternal and fetal blood and other body fluids.
    3
    Late-onset and nosocomial infections
    Occur due to:
  • Maternal contact
  • Contact with hospital personnel (cross infection)
  • Contact with inanimate objects.
    The most common causative organisms are:
  • Klebsiella
    spp.
  • Escherichia
    coli
  • Coagulase-negative staphylococcus
  • Staphylococcus aureus
  • Pseudomonas aeruginosa.
    3
    Risk factors for nosocomial infection are:
  • Low birthweight with a depressed immunological function
  • Underlying disease
  • Raised gastric pH and poor nutritional status requiring total parenteral nutrition
  • The excessive use of antibiotics
  • Multiple IV site access, the presence of an endotracheal tube and central lines
  • Long hospital stay
  • Poor compliance of staff with infection control, and poor hand washing
  • Shared equipment, overcrowding, and inadequate staffing
  • The presence of opportunistic organisms.
    1
    ,
    2
    Defences
    The physical defences
  • The skin
  • Mucous membranes
  • Gastric secretions
  • Tears
  • Urine pH
  • Ciliated epithelium.
    Are all affected by immaturity, poor skin keratinization, and invasive procedures.
    CHAPTER 23
    Care of the newborn
    600
    The non-specific defences
    • Phagocytes (neutrophils and monocytes)
    • Natural killer cells
    • Inflammatory responses
    • Antimicrobial proteins
    • Complement activation
    • Serum opsonins
    • Polymorphonuclear neutrophils.
      All of these are immature as there is little or no transmission via the pla- centa. Their ability to release complement is reduced until 6–18 months. This deficiency in phagocytosis and opsonization is pertinent in the case of GBS and is further compounded by prematurity.
      T and B cells
    • Generated from bone marrow.
    • T cells are responsible for cell-mediated immunity.
    • B cells confer humoral immunity from which antibodies are produced.
      Humoral immunoglobulins
      There is some evidence of transfer, which gives the newborn some pro- tection:
    • Maternal IgG
      is transferred from 22 weeks and increases by 30 weeks, giving the fetus passive immunity.
    • IgM
      does not cross the placenta, so immunity to acute maternal infection at the time of delivery is not provided.
    • IgA
      is secretory, present in saliva, sweat, tears, intestinal secretions, and colostrum.
      •
      IgD
      is present on the surface of lymphocytes to control activation and suppression of B cells.
    • IgE
      is present in low quantities in the serum but in higher quantities in the respiratory and gastrointestinal tracts.
      1
      ,
      2
      Signs of neonatal infection (Table 23.1)
      2 Early detection is crucial or the infection will overwhelm the baby leading to:
    • Septicaemia
    • Meningitis
    • Death.
      Indicators may be apparent in the maternal history, such as:
    • Maternal pyrexia
    • Prolonged rupture of membranes.
    • Length of gestation of the fetus.
      The midwife or nurse caring for the baby will often ‘feel’ that the baby is ‘not as well as it was’
      .
      Neonatologists in practice will act on this obser- vation, especially if it comes from an experienced neonatal nurse, and it often leads to examination and an infection screening.
      1,2
      NEONATAL INFECTION
      601
      Table 23.1
      Signs of neonatal infection
      Common signs Uncommon signs
      Pallor Purpura
      Poor feeding Omphalitis
      Tachycardia/arrhythmia Vasomotor instability Decreased peripheral perfusion Bleeding
      Unstable blood pressure Pustules
      Abdominal distension Bulging fontanelle
      Apnoea Splenomegaly
      Lethargy Rash
      Hyperbilirubinaemia Diarrhoea
      Recession/grunting/cyanosis Seizures Tachypnoea
      Unstable temperature
      Investigations
  • Surface swabs
    taken from multiple sites are useful when late infection is
    suspected or on admission to the NICU. The optimal site is a deep ear
    swab or a swab of obvious lesions in later-onset infection.
  • Blood cultures
    are mandatory before starting antibiotics.
  • Total neutrophil count
    is more reliable than a total white cell count. The immature to total ratio is a good indicator of infection.
  • CRP
    : a level of >6 mg/L is a sign of infection. This is used to measure the course of infection and response to treatment. Levels should return to normal 96h after starting treatment.
  • Platelet count
    : due to increased destruction, aggregation and adhesion occur, but this is usually a late finding in about 50% of cases.
  • CSF
    : lumbar punctures are carried out to rule out bacterial meningitis.
    • The sample should be clear.
    • CSF white cell level
      <30mm,
      3
      with more than 66% neutrophils.
    • CSF protein level
      of >1g/L in a term baby or 2g/L in a premature baby are suspicious of meningitis.
    • CSF glucose level
      should be approximately 70–80% of the plasma glucose level.
  • Urine
    : usually collected as a bag sample or suprapubic tap. The long- term effects of urinary infection can be renal scaring and atrophy.
    1
    ,
    2
    Management of the infected infant

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