The collapsed neonate
Whilst the definitive management of a critically ill neonate involves complex therapeutic interventions delivered by teams led by neonatologists, the geography of modern living dictates that a collapsed neonate may present to any acute care facility across the country which may have very limited medical, nursing, and anaesthetic resources. Seemingly well neonates may have been discharged home, within hours to days of birth, to remote, rural or island communities, and medical teams in those areas may have to deliver fundamental neonatal intensive care for a considerable period of time before a transport team can retrieve the patient. This discussion serves to outline the key diagnoses presenting in the collapsed neonate and what interventions could be offered by the anaesthetic team whilst awaiting retrieval.
1 Recognize the common presenting features in a collapsed neonate and identify the likely causes
2 Commence an appropriate therapy
3 Stabilize the child whilst awaiting the retrieval team arrival.
2D01; 2D07
You are fast-paged to your small district general hospital’s ED, immediately following the arrival of a term 10-day-old, previously well female neonate brought in by the paramedics in a collapsed state. On arrival, you find the patient to be intermittently gasping, with apnoeic pauses, peripherally cyanosed, and drowsy.
The key factors to consider when formulating a differential diagnosis include:
◆ Age: by definition of being under 28 days old, this patient is a neonate; however, certain pathologies are more likely within certain time frames of the neonatal period. Within the first few hours or days of birth, severe congenital anatomical anomalies are likely to manifest, e.g. tracheo-oesophageal fistulae or diaphragmatic herniae, presenting with respiratory distress or impaired feeding. At around days 7–14 of age, the initial physiological closure of the ductus arteriosus is subsequently followed up by the anatomical duct closure. This is a key development, resulting in the manifestation of duct-dependent cardiac lesions. Sepsis and metabolic disorders may manifest at any time throughout this neonatal period but tend to initially present with non-specific symptoms, including poor feeding, drowsiness, and apnoeas
◆ Apnoea: this is a non-specific sign which is likely to be present in any unwell neonate, independent of the presence or absence of respiratory pathology. Immaturity within neural pathways and vagal predominance result in any systemic stress, triggering apnoeas. Also, the respiratory reserve is severely limited in neonates, and an increase in the metabolic oxygen demand will be met initially by tachypnoea, which can only be sustained in the short to medium term and will subsequently progress to hypopnoea and apnoeas, due to respiratory muscle fatigue
◆ Peripheral hypoperfusion: similarly, this is a non-specific sign which is likely to be present in patients with respiratory, cardiovascular, septic, and metabolic pathologies. An early presenting feature of neonatal illness reported by parents is an inability to feed which often precedes hospital presentation by several days. In patients with respiratory pathology, this inability to feed results from the fact that they cannot sustain an adequate respiratory function via nasal breathing during feeding. With cardiac or septic pathologies, the infant cannot meet the metabolic demand during feeding, as this is an energy-demanding process in itself. The net result is that poor feeding for several days results in hypovolaemia and a calorie deficit, often manifest as failure to regain birthweight or further weight loss.
The differential diagnosis in this patient would be:
◆ Congenital cardiac anomaly: duct-dependent lesions will present at 1–2 weeks of life with peripheral hypoperfusion and cyanosis. Signs of heart failure may be present
◆ Sepsis: group B streptococcal infection from perinatal materno-fetal transmission. This may present as generalized septic shock or meningitis. A history of group B streptococcal status is usually available from the mother if she has undergone routine antenatal care
◆ Metabolic disorder: the potential specific diagnosis within this broad category is beyond the scope of this text, lying firmly in the remit of neonatal specialists. However, these disorders will generally present with a non-specific collapse, resembling neonatal sepsis and universal hypoglycaemia, and may be accompanied by seizures.
The patient’s ventilation is immediately supported with manual ventilation via an appropriate bag and mask, and monitoring is applied. Initial observations demonstrate a HR of 180, NIBP of 45/25 mmHg, and peripheral capillary refill of >5 s. A capillary blood sample reveals a blood glucose of 1.2 mmol/L, pH of 7.10, PaCO2 of 9 kPa, PaO2 of 5 kPa, a base deficit of –6 mol/L, and lactate of 4 mmol/L.
These results indicate tachycardia, hypotension, and a mixed metabolic and respiratory acidosis, all of which are compatible with a cardiac, septic, or metabolic pathology so, at this stage, do not aid with specifying the diagnosis. However, the initial resuscitation principles are the same, irrespective of the diagnosis:
◆ Physiological parameters: the normal range for the HR in a newborn is 140–160 bpm, but rates of 180–190 are commonly observed when the child is upset. Rather than noting the systolic and diastolic BPs, it is often more helpful to consider the MAP in neonates. This should equate to the gestational age in weeks for the first few months of life; for example, this patient with a gestational age of 41 weeks should have an MAP of 41 mmHg, so he is hypotensive with her current MAP of 32 mmHg
◆ Blood gas results: whilst most anaesthetists are familiar with the interpretation of arterial samples, a re-adjustment of normal values is required for capillary samples. A mild respiratory acidosis is expected with elevated PaCO2 and decreased PaO2 values, compared to arterial sampling. However, the base deficit and lactate should be within normal limits, with values outwith suggesting a metabolic component to the blood gas disturbance.
Interventions required include the provision of respiratory and cardiovascular support, the treatment of acidosis and hypoglycaemia, specific therapies to cover potential diagnoses, and referral for definitive care.
◆ Respiratory support: this patient’s airway may be threatened by virtue of an impaired consciousness, but she is likely to require urgent intubation and ventilation for respiratory support. In the short term, ventilation may be augmented with either a T-piece during periods of spontaneous effort or a neonatal self-inflating bag during apnoea. The application of positive pressure through both of these devices will lead to gastric insufflation, and early NG or orogastric tube insertion should be performed to minimize abdominal distension and diaphragmatic splinting
◆ Cardiovascular support:
• Access: securing IV access in neonates often presents considerable challenges to the anaesthetist. Veins are often easily visible through the relatively transparent skin but are typically difficult to cannulate, due to their small bore, tortuous pathway, and fragility. The dorsum of the hand or foot are reasonable sites for first attempts, and the long saphenous vein often affords a relatively consistent position, anterior to the medial malleolus, even when it cannot be seen. Scalp veins are often cannulated by neonatologists but can be difficult to secure, rendering them liable to displacement during resuscitation and transport. In the collapsed neonate, due consideration to intraosseous cannulation should be given early in the resuscitation phase, both with manual and automated systems, minimizing the risks of multiple access attempts and hence prolonging the periods of hypotension and hypoglycaemia whilst exacerbating hypothermia. Note the umbilical venous approach for central cannulation is only available to neonatologists in the immediate post-natal period and is not an option for anaesthetists, even if the umbilical cord clamp is still on when the patient presents
• Fluids: the presence of tachycardia, hypotension, and peripheral capillary shutdown necessitates fluid therapy; however, whilst administering fluid boluses, it should be borne in mind the potential for congenital cardiac pathology with the risk of excessive fluid replacement precipitating acute heart failure. In initial stages, a bolus of 20 mL/kg of normal saline is appropriate, with further boluses of 10 mL/kg titrated, depending on the trends of the cardiovascular parameters over at least 15 min following a fluid bolus. Glucose-containing fluids should never be administered as a volume bolus; however, this patient does require a loading dose of glucose as therapy for hypoglycaemia, and 2 mL/kg of 10% glucose, as per advanced paediatric life support (APLS) guidelines, with subsequent treatments, as necessary, following a recheck of blood sugar levels
• Inotropes: a broad-spectrum sympathomimetic agent is indicated in the collapsed neonate. Dopamine is often used in paediatric and neonatal units, in dose ranges of 5–20 micrograms/kg/min. Many anaesthetists are more familiar with the use of adrenaline infusions in the resuscitation phase of adults and children, and this is equally appropriate in the management of a collapsed neonate. The dose range is 0.1–1 micrograms/kg/min. Agents, such as noradrenline or dobutamine, are rarely indicated as first-line therapies and should only be considered on the advice of a neonatologist. As with all drugs, but particularly drug infusions, great care must be exercised when preparing these agents, as the dilutions and concentrations will be unfamiliar to many staff, and cross-checking of the prescription and preparation of these infusions is advised
◆ Anaesthesia: the collapsed neonate is likely to require anaesthesia during the resuscitation phase to facilitate ongoing interventions, controlled ventilation, and transport to definitive care. This should not be performed until volume resuscitation is well under way, multiple ports of venous access have been secured, and the appropriate staff, equipment, and drugs have been prepared, in anticipation of further deterioration
• Equipment: the equipment required to anaesthetize a 3 kg neonate is no different to that required for a 100 kg adult, and all national guidelines on skilled assistance, pre-use checks, and monitoring standards are equally applicable. Either cuffed or uncuffed tracheal tubes are suitable, with no evidence to suggest a higher complication rate from microcuffed tubes, which are sized from 3.0 mm upwards. The laryngoscope blade is the choice of the individual anaesthetist, but straight blades, e.g. a Robertshaw blade, are often favoured, although MacIntosh zero blades are effective for neonatal intubation. Ventilators, often stocked in EDs, are generally unsuitable for neonatal ventilation, due to excessive deadspace in the circuits and the inability to deliver small tidal volumes
• Drugs: commonly used induction agents, such as propofol and thiopentone, will be likely to cause significant hypotension, even in reduced dosing, if administered to the collapsed neonate. Etomidate is not used in neonatal or paediatric practice. The ideal induction agent in this clinical situation is ketamine, administered IV, at a dose of 1–2 mg/kg. This will provide an acceptable plane of anaesthesia, without compromising the BP. Midazolam and fentanyl may also be used as adjuncts, but caution should be applied, unless familiar with the use of these agents in sick children. Suxamethonium is still the recommended muscle relaxant, in doses of 1–2 mg/kg, to provide muscle relaxation for intubation, being mindful that fasciculations are usually not observed in small children. Bolus doses of adrenaline (1 microgram/kg) and atropine (20 micrograms/kg) and saline fluid boluses should be prepared and be immediately ready prior to induction. Where there has been an unsatisfactory response to 40–60 mL/kg of fluid boluses, commencing an adrenaline infusion prior to induction is recommended.
The patient fails to respond adequately to 40 mL/kg of saline boluses and is still requiring intermittent manual ventilation for progressive apnoeas. One IV line and one intraosseous line have been sited, and an adrenaline infusion has been commenced at 0.2 micrograms/kg/min. Benzylpenicillin and gentamicin have been administered. Anaesthesia has been induced with 2 mg/kg of ketamine and 2 mg/kg of suxamethonium, and a size 3.5 tracheal tube has been inserted without difficulty. The paediatric intensive care retrieval team have been called to transport this patient to the paediatric ICU (PICU); their arrival time is estimated at 2 hours.
The referring team is required to deliver paediatric intensive care until the arrival of the retrieval team. This is a standard of care, as outlined by the Royal College of Anaesthetists, and there should be appropriate staffing, equipment, training, and governance systems established to ensure that an appropriate standard of care can be delivered. The key principles of paediatric critical care delivery are best outlined on a systems basis:
◆ A—airway: the tracheal tube position must be securely fixed, ideally with zinc oxide tapes, over the maxillary regions, rather than tube ties which often let smaller tubes slip. The tube should be suctioned with a soft suction catheter; the appropriate size is double that of the internal diameter of the tracheal tube, e.g. a 7F catheter for a 3.5 mm or a 10F catheter for a 5 mm tube
◆ B—breathing: unless a paediatric-specific ventilator is available, it is likely that manual ventilation will be required. A problem with adult ventilators is that they are unable to deliver appropriately small tidal volumes without excessive pressures and that the volume of the pressure-monitoring apparatus prevents an adequate tidal volume. As such, hand ventilation may be the optimal strategy, either with a T-piece or a self-inflating bag. Capillary or venous blood gases should be checked at the commencement of ventilation and at around 30-min intervals, and ventilation rates titrated accordingly. Whilst neonatal practice is to avoid delivering 100% oxygen, this is acceptable in the short-term situation, and the use of oxygen–air blenders, or other similar devices, should only be undertaken where appropriate expertise is available. A CXR should be performed after intubation to confirm the tracheal tube position. A gastric tube should be inserted in all patients for drainage of any gastric insufflation that may impede an efficient ventilation
◆ C—circulation: additional 20 mL/kg boluses of saline may be administered, as required, for hypotension, although, if >80–100 mL/kg are required, the haematology profile should be checked, as haemodilution is likely and blood or platelet transfusions may be indicated. In all patients, maintenance fluids should be administered, using the 4–2–1 mL/kg/hour formula where 4 mL/kg/hour is administered for the first 10 kg of body weight, plus 2 mL/kg/hour for a body weight of 10–20 kg, and an additional 1 mL/kg/hour for any body weight over 20 kg, if necessary. In this 3.5 kg patient, the maintenance infusion rate would be 14 mL/hour. The exact composition of the fluid may be dependent on local or regional guidance, but an isotonic mix of saline and glucose is recommended. It is important that dextrose is a component of maintenance fluids; otherwise, hypoglycaemia is a likely consequence. The adrenaline infusion should be titrated to a rate achieving an MAP comparable to the patient’s post-conceptual age in weeks. Any points of venous or osseous access should be well secured. Central venous or arterial access is not normally indicated in this stabilization phase, unless staff with the appropriate skills are present
◆ D—disability/neurology: it is vital that the patient remains adequately sedated and relaxed during the stabilization and transport phase. Inadequate sedation may trigger tachycardia and hypertension that may be misinterpreted as cardiovascular instability. Inadequate relaxation will allow coughing which may displace the tracheal tube, trigger profound vagal reflexes, and will certainly impede effective ventilation. The standard infusions used are morphine, midazolam, and a relaxant such as vecuronium or rocuronium. These should all be prepared, according to local monographs, and be double-checked before administration to the patient. The standard infusion rates are morphine 20 micrograms/kg/hour, midazolam 0.1 micrograms/kg/hour, and vecuronium 0.1 mg/kg/hour, though these should always be discussed with the PICU team before commencing, and the infusion rates titrated to response. Pupillary responses should be checked at regular intervals
◆ Environment: attention should be paid at all times to maintaining the environmental temperature to mitigate hypothermia in the neonate. Ideally, the ambient air temperature should be turned up to 26–28°C, though this may prove uncomfortable for staff. Forced air warming devices should be used, wherever possible, and prolonged periods with the skin exposed, e.g. for a central line insertion, should be avoided. Preparation for the retrieval team arriving includes ensuring all notes and prescriptions are documented and copies are made of the relevant paperwork.
Summary
The management of a collapsed neonate is a challenging situation that may present at any acute-receiving facility, including those without inpatient neonatal and paediatric services. It is the responsibility of the ED and anaesthesia team to resuscitate and stabilize these patients prior to the arrival of the retrieval team. Neonatal collapse may be due to complex cardiac, septic, and metabolic pathologies; however, the core treatment principles should be initiated which will optimize the condition of the neonate prior to transfer, including:
◆ Early recognition of the acutely unwell neonate: detection of apnoeas, poor peripheral perfusion, drowsiness
◆ Prompt intervention to stabilize cardiorespiratory decompensation: manual respiratory support; early IV or intraosseous access with fluid boluses; inotropic infusion; anaesthesia and intubation, if failing to respond to initial therapies
◆ Stabilization and preparation for retrieval team transport: securing tubes and lines; assessing the adequacy of ventilation; maintaining the fluid balance and glycaemic status; preventing hypothermia.
Kattwinkel J, Perlman JM, Aziz K, et al.; American Heart Association (2010). Neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics, 126, e1400–13.
Paediatric Intensive Care Society (2010). Standards for the care of critically ill children, 4th edn. Available at: <http://www.ukpics.org.uk/documents/PICS_standards.pdf>.