A SHOCKED NEONATE
History
Freddie is 3 days old. He is brought by ambulance to the resuscitation room in A&E. He was found in his cot this morning looking mottled and breathing very fast. He had been well until yesterday when he did not feed as well as usual. He was born at 39 weeks’ gestation by normal vaginal delivery in a midwife-led birthing unit and was discharged home the same day. There was no prolonged rupture of membranes and he did not require any resuscitation at birth. He has been exclusively breast-fed. He did not receive vitamin K due to parental objection.
Examination
Freddie is grunting and has a respiratory rate of 70/min with subcostal, intercostal and sternal recession. His lung fields sound clear. Oxygen saturation monitoring does not pick up a trace. He looks mottled, cyanosed peripherally and his limbs feel cold. Capillary refill time is 5 s, heart rate is 180/min, blood pressure is unrecordable, and the femoral pulses cannot be felt. The heart sounds are unremarkable. The liver edge is palpable 3 cm below the costal margin and his temperature is 35.0C.
INVESTIGATIONS
Arterial blood gas
pH 7.01 7.35–7.42
PaCO2 5.3. kPa 4.7–6.0
kPa PaO2 8.1
kPa 9.3–13.3
kPa HCO3 10
mmol/L 18–20
mmol/L Base excess 18 2.5 to 2.5
mmol/L Glucose 3.8 mmol/L 3.3–5.5 mmol/L
Questions
• What is the interpretation of the blood gas result?
• What is the most likely diagnosis and what is the differential?
• What is the initial management of a collapsed neonate?
Medicine
The pH is 7.01, which is a severe acidosis. The PaCO2 is normal, so the acidosis is not respiratory in origin. The low bicarbonate and large negative base excess indicate that this is a metabolic acidosis. There is also a degree of hypoxaemia. The baby’s circulation is so poor that pulses are not palpable, the saturation meter cannot pick up a pulse trace and a severe metabolic acidosis has developed due to hypoperfusion. This is most likely to be a case of cardiogenic shock due to a congenital left heart obstructive lesion. The clues are in the age of the baby and the absence of the femoral pulses. Left-sided obstructive cardiac lesions rely on the ductus arteriosus to perfuse the systemic circulation by passage of blood from the pulmonary arteries into the distal end of the aortic arch. As the ductus arteriosus closes, the systemic perfusion becomes dramatically reduced, resulting in collapse and shock. Freddie actually had hypoplastic left heart syndrome (HLHS). The absence of a murmur does not rule out a cardiac cause, and murmurs are not always present in HLHS.
Congenital cardiac lesions presenting with neonatal collapse
• Severe aortic coarctation
• Aortic arch interruption
• Hypoplastic left heart syndrome
• Critical aortic stenosis
Differential diagnosis of a collapsed neonate
• Infection – e.g. group B Streptococcus, herpes simplex
• Cardiogenic – e.g. hypoplastic left heart syndrome, supraventricular tachycardia
• Hypovolaemic – e.g. dehydration, bleeding
• Neurogenic – e.g. meningitis, subdural haematoma (‘shaken baby’)
• Lung disorder – e.g. congenital diaphragmatic hernia (late presentation)
• Metabolic – e.g. propionic acidaemia, methylmalonic acidaemia
• Endocrine – e.g. panhypopituitarism
In any collapsed neonate, it is essential to adopt a standard approach to resuscitation. The airway should be maintained, high-flow oxygen administered, intravenous access obtained and fluid resuscitation should be given for the shock. Blood glucose measurement must be checked early and corrected if low. A blood gas sample should be analysed. Intravenous antibiotics should be given promptly as sepsis is a possible treatable cause. If there is any suspicion of a duct-dependent cardiac lesion, a prostaglandin infusion should be commenced, as this is life-saving. Early involvement of senior paediatricians, an anaesthetic team and paediatric intensive care services will help appropriate management.
KEY POINTS
• Congenital cardiac disease can present as shock in a neonate after several days.
• The absence of a murmur does not rule out congenital heart disease.
• A prostaglandin infusion can maintain patency of the ductus arteriosus and can be life-saving.
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