The collapsed neonate is a presentation that may require urgent intervention outside specialist centres. This can be considered as the sudden deterioration, including arrest, of a child that was apparently healthy at birth. The presentation is usually in the first 7 days.
There are some additional diagnoses that are important:
Endocrine: Adrenal insufficiency. Hypothyroidism
Respiratory tract infection
Sepsis within the first week of life is a serious condition with high risk of morbidity and mortality. Some key pathogens include:
Group B strep
As is the case in many age groups, but even more so here, the presentation is often non specific. Key features that may suggest this as a diagnosis include:
Temperature change - >38.5 or <36
Heart rate change - >180 or <100
Tachypnoea - >50 bpm
Leukocytosis - > 34x10^9/L
Congenital Heart Disease
This is an important potential pathology and is considered in more detail elsewhere. Key features that may support this as a diagnosis include:
Cyanosis - refractory to oxygen
Tachypnoea - especially in the absence of lung pathology
Absent femoral pulses
Lactic acidosis unresponsive to initial resuscitation
CXR changes - Cardiomegaly and pulmonary oedema
The major CHD phenotype that is of concern in the collapsed neonate is ‘duct-dependent’ CHD. Here, the patent ductus arteriosus had been masking whatever serious underlying CHD lesion the child had, by allowing mixing across the sides of the circulation, and as it closes, the problems can suddenly manifest themselves.
There are a wide range of metabolic disorders that can affect neonates, and thus a wide range of presentations. Some key ones to consider include:
Inborn errors of metabolism
Fatty acid oxidation defects
Congenital adrenal hyperplasia
Urea cycle defects
Glycogen storage disorders
Key features that may suggest this as a cause of neonatal collapse are generally those of a multi systemic nature, including:
These problems are also more common in children with consanguineous parents.
Despite the extensive number of potential causes, establishing the ammonia level in a potentially metabolic cause of collapse is essential. This is because of the notable toxicity of it to the developing brain, which is related to both the degree and duration of the elevation. Lowering this is therefore a time-critical management task.
This remains a clear consideration for all pediatric presentations. This is discussed in more detail elsewhere. A clear exploration of the history and careful examination of the child is essential here. Essentially any injury in a neonate is going to be caused by someone else, because of their development level. Injuries can very rapidly lead to compromise in these children because of the
Consider exploring the history of administration of vitamin K at birth, as hemorrhagic disease of the newborn is a parallel consideration in some presentations.
Certain factors in the history can provide useful information on the underlying cause. Features to consider exploring include:
Pathogens in mother - Group B strep, HSV
Gestation at delivery
Mode of delivery
Risk factors for sepsis
Any hereditary disorders
Sudden infant death
Other illness at home
These patients can often present in extremis. A systematic approach is therefore advocated, as usual, generally an A to E approach, treating life-threatening issues as they are encountered.
Airway Airway support may be needed. This may be due to the presentation or treatment e.g. prostaglandin infusion can lead to apnoeas, so I&V should be considered in this group (>15mcg/kg/min). Intubation should be undertaken by an appropriately skilled operator in a safe environment. Resuscitation of the patient should be optimised prior to induction of anaesthesia for intubation. There should also be anticipation of possible CVS instability, with preparation for this, with emergency drugs available.
Breathing The respiratory status of the patient should be considered. This will include standard features of assessment:
SpO2 - pre and postductal
Work of breathing
Lung field auscultation
Blood gas analysis
Provision of supplemental oxygen should be given to target SpO2 values of >95%. In cases of PDA dependent heart disease, there may remain hypoxia resistant to oxygenation, and indeed, oxygen is a potent trigger for duct closure. Target oxygenation in these patients is usually 75-85% to reduce the impact of oxygen on duct closure. Insertion of a gastric tube may allow decompression of the stomach to aid ventilation. A CXR should be performed to provide information on lung fields, heart size and OETT position.
Pulses - comparing at different sites
Two points of IV access should be obtained, with IO access if this is challenging and causing a delay (there is an argument for using this straight away). Fluid resuscitation (initially 10ml/kg crystalloid) is usually appropriate in most of these presentations. The addition of pharmacological support of the circulation with adrenaline infusion may be considered. Central access may be considered in sick patients, although this may remain a specialist skill, outside of the scope of non-paediatric specialists. Peripheral lines (and indeed IO access) can be used for most infusions in the interim. Consider insertion of an arterial line if the skills are available. Similarly, if there are skills available locally to perform an echocardiogram, this can provide very useful information.
Good rule of thumb values for the neonate are 60/30 (40) mmHg.
Sedation will need to be commenced to tolerate IMV if this has been needed, and will usually entail morphine and midazolam (although midaz may not be needed). Pupils and glucose levels should be measured regularly. Phenobarbitone (20mg/kg) is the anticonvulsant of choice in this age group. The collapsed state is a contraindication to performing a lumbar puncture so suspected meningitis is treated clinically. Hypoglycaemia can be corrected with 10% glucose 2ml/kg.
Inflammatory markers - may not be elevated in neonatal sepsis
Meningococcal and HSV PCR
Patients can get cold very quickly and temperature should be maintained, either through caring for them in a resuscitaire or maintaining covering. Despite this, a thorough examination is still important.
The assessment of the metabolic patient can include a number of investigations. Hypoglycaemia screen (best taken when hypoglycaemic):
Urine: ketones, inorganic acids
Plasma amino acids
Urine: ketones, organic and amino acids, orotic acid.
Fluid therapy will be commenced, with a max of 100ml/kg/day recommended because of the SIADH risk. This inclusion of glucose in this is important.
Part of the management will follow the above systematic review. The involvement of the appropriate specialist teams can be very helpful in these situations. There is a network of critical care retrieval teams in the UK that can be an excellent source of advice here.
Antibiotics The challenge of diagnosing sepsis and the significant impact of it mean that there is a very low threshold for giving antibiotics in a collapsed neonate. There is little that can provide good positive or negative predictive value, and so ‘cover’ is usually given. This will tend to be cefotaxime and amoxicillin IV. This may need alteration if there is an increased likelihood of nosocomial pathogens.
Strong consideration should also be given to IV acyclovir to cover for HSV infection, for much the same reasons.
Duct-Dependent CHD The specific goal in these patients is to reopen the ductus arteriosus, and return the child back to the circulation that it had before, where it was apparently fairly stable. This is of course a temporising measure, but can allow time for specialist input. This will usually entail a prostaglandin infusion. There are differing doses for ‘opening’ and ‘maintaining’ duct patency, and in the collapsed neonate, it is the opening that is required. This needs a higher dose: starting at 20ng/kg/min, and titrating up rapidly if needed (can go to 50 and then even 100 if needed).
It is important to note that these are not the only potential CHD lesions in the collapsed neonate, and so specialist input is essential. Some patients require urgent surgical intervention, and will derive little benefit, or even adverse effects, from such supportive measures.
Ammonia Establishing the ammonia level in a potentially metabolic cause of collapse is essential. This is because of the notable toxicity of it to the developing brain, which is related to both the degree and duration of the elevation. Lowering this is therefore a time-critical management task. Initial management involves cessation of all protein intake and administration of IV glucose and intralipid.
There are a range of specific treatment options for these patients, which is best guided by a specialist. The British Inherited Metabolic Disease Group have some useful emergency guidance. http://www.bimdg.org.uk/site/index.asp