Breathing problems in the newborn

11.3 Breathing problems in the newborn



Luke Jardine, Mark Davies



Introduction


The establishment and maintenance of breathing is vital for the newborn infant. Problems with breathing are common and dealing with them forms the bulk of neonatal care. The establishment of lung function is dealt with in Chapter 11.1. Respiratory problems beyond the immediate post-birth period include respiratory distress (from a myriad of causes), airway obstruction and hypoventilation (including apnoea and various neuromuscular problems).



Respiratory distress


Respiratory distress is a broad term that refers to a constellation of signs seen in the neonate who has difficulty breathing and has increased respiratory effort. The signs that the infant with respiratory distress exhibits include the following:



• Tachypnoea – is defined as a respiratory rate of more than 60 breaths per minute. In order to clear more carbon dioxide, the infant increases the respiratory rate and therefore the minute ventilation.


• Expiratory grunt – this sound is produced by the exhalation of gas from the lungs through a partially closed glottis; this helps with the maintenance of the functional residual capacity. It can be misinterpreted by the inexperienced observer as the baby crying or moaning.


• Recession – with increased inspiratory effort the baby generates more negative intrapleural pressure. This increases the gradient between the atmosphere and the intrapleural space. This gradient occurs across the chest wall, and the softer or more compliant parts of the chest wall are sucked in during inspiration – usually the intercostal spaces and the sternum (the lower part is especially mobile and can be sucked in considerably during inspiration). There is also indrawing of the lower costal margin during inspiration, but this occurs owing to a different mechanism, namely contraction of the diaphragm, and is sometimes erroneously called subcostal recession.


• Nasal flare – the alae nasi flare during inspiration and this decreases airway resistance.


• Central cyanosis – almost invariably some alveoli that are not ventilated remain perfused. The resultant ventilation/perfusion mismatch leads to cyanosis. It is important to remember that babies who are relatively polycythaemic will have cyanosis at relatively high oxygen saturation, and babies with low haemoglobin will not appear cyanosed until their saturation is extremely low.


Not all babies with respiratory distress have all of the signs listed above. For example, an infant may have significant respiratory distress and yet have a respiratory rate of 40 breaths per minute. Often, the somewhat more subjective impression that the baby has increased respiratory effort or is ‘working hard’ is just as important.



General principles of management of respiratory distress


The general principles of management apply no matter what the diagnosis or gestational age. The causes of respiratory distress are many, and some are immediately life-threatening. As always, you must attend to any need for resuscitation and ensure that the infant is physiologically stable.



• Put the baby somewhere you can watch it. This is best achieved by admission to a neonatal nursery with the baby nursed in an incubator, unclothed initially (this allows frequent observation and the status of the baby’s breathing and colour can be assessed instantly upon looking in the incubator). The incubator should also keep the baby warm.


• Monitor the vital signs including heart rate, respiratory rate and pre-ductal oxygen saturations (put the oximeter probe on the right hand). These should be noted frequently so that any changes over time can be determined with a glance at the observation record.


• Assume the baby is infected until the results of investigations confirm or exclude this. Take cultures: a blood culture is best, with or without surface swabs and a gastric aspirate. Then start antibiotics.


• Start intravenous fluids. If you are struggling to breathe you do not need a stomach full of milk. If a peripheral venous cannula cannot be readily inserted then insert an umbilical venous line. Infusing 10% dextrose at 60 mL/kg daily is more than adequate in the first couple of days of life.


• Get a chest X-ray. There are some conditions that require an immediate change in management, such as a pneumothorax, congenital diaphragmatic hernia or intrapleural fluid. Although many conditions have characteristic appearances on chest X-ray, none of the findings is definitive. You can never exclude infection by looking at a chest X-ray.


• Get advice. If you are not in a neonatal unit that has a paediatrician or neonatologist then you should ring your local neonatal unit. Do this after attending to any requirements for resuscitation and after you have started antibiotics.


The baby may require respiratory support for the respiratory failure that accompanies the respiratory distress. This may include oxygen therapy, continuous positive airway pressure (CPAP) or intubation and mechanical ventilation. Some specific lung diseases will also require exogenous surfactant treatment.



• Oxygen treatment. Remember that oxygen is a toxic substance, so use only the minimum amount necessary. If pre-ductal oxygen saturations are below 90%, it is reasonable to increase the fraction of inspired oxygen (FiO2). In infants who do not require any other form of respiratory support this is best achieved by running oxygen into the incubator. Start with a flow of 2 L/min and increase or decrease to keep the pre-ductal oxygen saturations in the low 90s.


• Blood gas monitoring. Usually, if an infant requires an FiO2 of more than about 0.4 on CPAP or is intubated and ventilated, they should have an arterial line. This is best achieved by inserting an umbilical arterial catheter, but this should be done by someone who is experienced in doing it. Get advice.


• Continuous positive airway pressure (CPAP). This is usually delivered with some form of nasal or nasopharyngeal tube. The aim is to provide a continuous positive background pressure to the infant’s airway to help keep the airway open, maintain good lung volume and treat any atelectasis. Usually, a pressure of around 7 cmH2O is used. This will help to minimize any ventilation/perfusion mismatch.


• Intubation and mechanical ventilation. The decision to ventilate a baby with respiratory distress needs to be taken in discussion with the relevant paediatrician or neonatologist. A baby with respiratory distress is at least breathing and achieving some gas exchange – you don’t want to convert that situation into something worse with multiple unsuccessful attempts at intubation.


• Generally accepted criteria for the need for ventilation are unresponsive, severe or frequent apnoea; acidosis (arterial pH < 7.25 with an arterial partial pressure of carbon dioxide (Paco2) > 60 mmHg or pH < 7.25 with base excess below − 10 not corrected by bicarbonate or volume loading), requiring a Fio2 > 50% to maintain oxygen saturation above 88%.

• Exogenous surfactant is usually given via an endotracheal tube to any intubated baby with hyaline membrane disease. Natural, animal-derived surfactants are usually used, including Survanta (a calf lung extract), Curosurf (a porcine product) and BLES (bovine lipid extract surfactant). It is also used before the diagnosis is made in infants of less than 26 weeks’ gestational age, as soon as they are intubated.


Once any necessary resuscitation has been attended to, the management principles above applied and any respiratory support given, you can think about working out a cause for the respiratory distress.



• Take a history. Get details of the pregnancy, labour and delivery: results of antenatal screening including ultrasound findings, poly- or oligo-hydramnios, gestational age, risk factors for infection, meconium-stained liquor, need for resuscitation after birth.


• Examine the baby: be gentle. Look for any obvious congenital abnormalities.


• Get a chest X-ray if you haven’t already done so. Take blood for a full blood count and film examination. A blood culture should already have been taken. Send a gastric aspirate and surface swabs (include groin and ear) for bacterial culture.


• If an airway problem is suspected, make sure the nares and oesophagus are patent. The successful passing of a nasogastric tube should confirm this.



Causes of respiratory distress


A wide variety of congenital and acquired disorders can present in the newborn period as respiratory distress (Box 11.3.1). A systematic approach, which includes taking a thorough history, performing a complete physical examination and undertaking ancillary investigations, will readily determine most of these. The most common causes are explained in greater detail below.



Box 11.3.1 Causes of respiratory distress




• Infection (e.g. congenital infection, acquired infection)


• Retained fetal lung fluid, also known as transient tachypnoea of the newborn or ‘wet lung’


• Infant respiratory distress syndrome, also known as hyaline membrane disease


• Pulmonary air leak (e.g. pneumothorax, pneumomediastinum, pneumopericardium, pulmonary interstitial emphysema)


• Aspiration (including meconium aspiration syndrome, blood, liquor amnii and milk)


• Surgical conditions (congenital diaphragmatic hernia, cystic hygroma, haemangioma, congenital lobar emphysema, congenital cystic adenomatoid malformation, sequestration of lung, lung cysts)


• Pulmonary hypoplasia (e.g. oligohydramnios from prolonged premature rupture of membranes or decreased fetal urine output, space-occupying thoracic lesions, fetal dyskinesia)


• Chronic neonatal lung disease


• Airway obstruction (e.g. choanal atresia, oesophageal atresia with tracheo-oesophageal fistula, micrognathia, laryngomalacia, tracheomalacia, vascular ring, subglottic stenosis)


• Cardiac disease (e.g. pulmonary hypertension, transposition of the great arteries with intact septum, total anomalous pulmonary venous return, patent ductus arteriosus, large ventriculoseptal defect, atrioventricular canal)


• Other respiratory causes (pulmonary haemorrhage, pulmonary lymphangiectasia, pleural/chylous effusions, hydrops fetalis, eventration of the diaphragm)


• Abdominal distension (e.g. bowel obstruction, necrotizing enterocolitis, massive ascites)


• Other – severe anaemia, polycythaemia, ischaemia, metabolic disease, increased metabolic demand such as hyperthermia, acidaemia, decreased chest wall compliance (e.g. severe oedema or skeletal dysplasia)


It is important to remember that not all cases of respiratory distress are caused by respiratory disease. One of the most common non-respiratory causes is metabolic acidosis (as seen in hypoxic ischaemic encephalopathy); the baby compensates for the acidosis by increasing the respiratory effort in order to clear more carbon dioxide. Some of the other non-respiratory causes of respiratory distress are listed in (Box 11.3.1.)



Respiratory causes of respiratory distress


Regardless of the lung disease that causes the respiratory distress, the single most important aspect of its pathophysiology is atelectasis. Almost all of the conditions listed below will have an element of lung atelectasis. Atelectasis decreases respiratory compliance and therefore increased pressure is required to achieve adequate tidal volumes. Atelectasis also leads to ventilation/perfusion mismatch and cyanosis. These features in turn lead to a need for increased ventilation and therefore respiratory distress.



Infection


It can be impossible to differentiate infection from other causes of respiratory distress such as respiratory distress syndrome, retained fetal lung fluid or meconium aspiration syndrome. Therefore, in all babies with respiratory distress, there should be a high index of suspicion for infection and a low threshold for septic workup and commencement of antibiotic therapy. Infection may be contracted in utero (congenital) and present at birth or soon afterwards (usually during the first 48  hours of life), or acquired and present later (this is often nosocomial). Maternal risk factors for congenital infection include known colonization with a pathogenic organism (e.g. group B streptococcus); previous infant with early-onset neonatal septicaemia; prolonged rupture of membranes (≥ 18  hours); multiple vaginal examinations; intrapartum or postpartum temperature ≥ 38°C; and preterm labour (< 37 completed weeks of gestation).


Signs of infection in the baby are non-specific and include respiratory distress, an unexpected need for resuscitation, lethargy, apnoea, hypoglycaemia, hyperglycaemia, bradycardia, poor perfusion, hypotension, increased respiratory tract secretions, temperature instability (especially hypothermia) and feed intolerance. Infection may be found in any normally sterile or non-sterile site, but is most commonly seen in the blood (septicaemia), respiratory tract, urinary tract or cerebrospinal fluid. A large number of organisms including bacteria, viruses and fungi have been reported to cause congenital and nosocomial infection in neonates.


Unless you are absolutely certain that the baby does not have a bacterial infection (and this is rarely the case in a baby with respiratory distress), you should start antibiotics. Antibiotic regimens vary according to local patterns of disease, the age of the baby and previous organisms isolated (from mother or baby). Generally speaking, initial antibiotic choices should be broad-spectrum and then tailored once an organism and its antibiotic sensitivities have been identified. For early infection, a penicillin and aminoglycoside are usually used. Antibiotic choice for late infection is very much driven by the type of bacteria prevalent in the neonatal unit at the time and known colonizing bacteria.



image Clinical example


Baby Caleb was born via vaginal delivery at 41  weeks and 5  days’ gestation. His 30-year-old primigravida mother had undergone induction for being post dates and had received two doses of dinoprostone (Prostin). An artificial rupture of membranes was performed 19  hours prior to delivery and no intrapartum antibiotics had been administered. Caleb was unexpectedly flat at delivery but responded well to 60  seconds of intermittent positive-pressure ventilation via bag and mask for resuscitation. His birth weight was 3200 g and the Apgar score was 4 and 8 at 1 and 5 minutes respectively. At 60  minutes of age he was noted to have grunting respirations, poor perfusion and seemed lethargic. Caleb was admitted to the nursery, had a full blood count and blood culture collected, and was commenced on intravenous antibiotics and a 10% dextrose infusion at a rate of 8 mL/h. He proceeded to have major apnoea, which required intubation and mechanical ventilation. Umbilical venous and arterial catheters were placed. Caleb continued to deteriorate with increasing oxygen requirements, hypotension and hypoglycaemia. At 14  hours of age the laboratory called to inform that the blood culture was positive and growing Gram-positive cocci. Despite intravenous antibiotics, inotropic support and mechanical ventilation, Caleb died at 20  hours of age. The culture subsequently revealed group B streptococcus, which was sensitive to penicillin.

Related posts:

  1. Sudden unexpected death in infancy
  2. Birth defects, prenatal diagnosis and teratogens
  3. Neural tube defects, large heads and hydrocephalus
  4. The newborn infant: stabilization and examination

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Aug 4, 2016 | Posted by in PEDIATRICS | Comments Off on Breathing problems in the newborn

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