Acute neonatal emergencies

The neonatal period

The neonatal period is one of profound physiological change, and although cardiorespiratory transition is largely completed shortly after birth, organ function and homeostasis continue to mature over the first month after birth. The neonate is thus uniquely vulnerable and may deteriorate rapidly with illness and physiological stress. In addition to postnatally acquired disease, neonates are at risk of vertical infection and may present with a wide range of congenital, genetic and metabolic disorders. With early discharge of mothers from perinatal centres, presentation of neonates to EDs in the first postnatal week is not uncommon. Although this is mostly due to minor problems, emergency physicians must be alert to a range of more serious conditions specific to the neonate. This chapter focuses on common medical and surgical emergencies in term neonates after the immediate birth transition.

Neonatal resuscitation (see Chapter 4.5 , Neonatal resuscitation)

Newborn life support focuses on the anatomic and physiologic adjustments needed to achieve the conversion from placental gas exchange to pulmonary respiration. The two key steps in this transition are initiation of air breathing and change from the placental to the pulmonary circulation as the source of cardiac preload, both of which require lung aeration. Thus, guidelines for resuscitation of the newborn emphasise airway and breathing, with a compression to breath ratio of 3:1 for cardiopulmonary resuscitation. However, evidence suggests that higher compression rates may be equally effective, and once the neonate has been discharged from a perinatal centre, use of paediatric resuscitation guidelines is appropriate, including 15:2 compression ratio. Nevertheless, attention to temperature control and blood glucose concentration remains important, and use of a T-piece device with oxygen blender in pulmonary resuscitation is recommended as this delivers controlled continuous end-expiratory positive pressure. The umbilical vein is useful for central access in the first few days after birth and often until the end of the first week.

Assessment of the neonate

Assessment of the unwell neonate should include review of the perinatal history, as this may contain clues as to possible diagnosis ( Table 4.4.1 ). Although antenatal ultrasound readily detects most major congenital malformations, there are several notable exceptions, such as transposition of the great arteries and coarctation. Feeding history is important, and it is useful to compare current weight with peak postnatal weight in assessing hydration. In term and near-term breastfed neonates, the nadir of postnatal weight loss typically occurs on days 3 to 4, with mean weight loss of 7–8%. Most newborns regain their birthweight by 10 to 14 days. Clinical signs that should not be missed include cardiac murmurs, reduced or absent femoral pulses, imperforate anus and genital abnormalities, wide or full antenatal fontanelle and palate defects. Mild cyanosis is difficult to detect clinically and may only be detected by pulse oximetry. By 24 hours of age, the mean pulse oximetry saturation in term and late preterm neonates is 97%, with a third centile of 94%. Pulse oximetry saturation of ≤94% warrants further assessment. Chest radiographs should be screened for skeletal abnormalities, especially rib and vertebral anomalies.

The collapsed neonate

The commonest cause of neonatal collapse is duct-dependent congenital heart disease. Sepsis must always be considered, along with other noninfectious, potentially life threatening, yet treatable causes ( Table 4.4.2 ).

Diagnoses such as duct-dependent congenital heart disease and inborn errors of metabolism can be difficult to differentiate from infection at the time of initial presentation. All of these conditions can present with nonspecific symptoms, such as lethargy, poor feeding or breathing difficulties. On examination, the neonate may appear grey, pale or cyanosed, be irritable or lethargic, and may have tachypnoea, tachycardia and poor perfusion. Hypotension is a very late sign. Early recognition, stabilisation and management of the critically ill neonate may be life-saving.

The structured approach to the resuscitation of the collapsed infant involves support of airway, breathing and circulation and is presented in Fig. 4.4.1 .

Sepsis

Infections represent an important cause of morbidity and mortality in the first month after birth. Critically unwell neonates should be presumed to have bacterial sepsis until proven otherwise and empiric antibiotics commenced. Neonates are particularly susceptible to bacterial infection due to suboptimal type 1 T helper cell responses and B-cell differentiation, resulting in reduced antibody production, especially to polyscaccharide antigens, and impaired cytotoxic T-cell and neutrophil function.

The signs and symptoms of sepsis may be quite subtle, and the duration of illness is variable, with some infants presenting after being unwell for several days and others deteriorating rapidly. Any one or combination of the symptoms, such as lethargy, irritability, respiratory distress, poor feeding, vomiting, diarrhoea or fever, may be a manifestation of sepsis. A fever in a neonate is defined as a temperature of ≥38°C. Fever is a very unreliable finding, as many septic neonates will be hypothermic. It is important to ask about perinatal risk factors for infection and infectious contacts (see Table 4.4.1 ).

On examination, the infant with severe sepsis is often pale, grey or cyanotic. The skin is usually cool and mottled due to poor perfusion. The infant may seem lethargic, obtunded or irritable. The vital signs including temperature, respiratory rate, oximetry, heart rate, capillary refill time and blood pressure should be obtained. Disseminated intravascular coagulopathy may develop in severe sepsis with petechiae or purpura and is usually associated with poor outcome. A complete physical examination is required to look for focal signs of infection. If meningitis is present, there may be a bulging or tense fontanelle with a high-pitched cry, although more commonly neonatal meningitis presents with nonspecific findings. If the infant has a respiratory infection there may be focal chest findings. It is important to examine for joint swelling and tenderness and to examine the umbilical stump for signs of omphalitis.

The goal of treatment in the ED is to support and stabilise the infant and to cover with antibiotics for serious bacterial infection such as bacteraemia, urinary tract infection, meningitis and osteomyelitis. In the collapsed neonate, immediate resuscitation with support of airway, breathing and circulation must be initiated. If the infant develops signs of shock, stabilisation includes fluid resuscitation and commencement of inotropic support.

A full septic screen should be initiated in any neonate with a fever or with clinical suspicion of sepsis. This includes full blood count, blood culture, urinalysis and urine culture (catheterised or suprapubic specimen), lumbar puncture and chest X-ray. A venous blood gas is important as it may show evidence of a metabolic acidosis and may reveal hypoglycaemia (blood glucose concentration <2.6 mmol/L). Serum biomarkers such as C-reactive protein and procalcitonin can be measured to aid in the diagnosis of serious bacterial infections in neonates. A coagulation profile should be performed if disseminated intravascular coagulation is suspected. Lumbar puncture should be postponed if the infant is too unwell to tolerate the procedure. When cerebrospinal fluid is obtained, it should be sent for cell count, Gram stain and culture, and molecular testing for herpes simplex virus and enterovirus.