Human parechovirus (HPeV)-3 is a newly recognised pathogen causing severe infections including sepsis-like illness, meningitis, encephalitis and a hepatitis-coagulopathy syndrome, especially in neonates and young infants.
“The infant was born at 28 weeks’ gestation, and deteriorated at one month of life with fever and abdominal distension and had evidence of intramural bowel gas on imaging. Parechovirus was subsequently isolated from naso-oropharyngeal and rectal swabs and he was managed medically with antibiotics and the cessation of enteral feeds.” (Angley et al., 2020).
“A 33-day-old pre-term (36 weeks of gestation) male infant was transferred to our institute with a 12 hour history of fever, lethargy and abdominal distention. He was admitted to the intensive care unit due to bradycardia and apnoea, which suggested septic shock. On admission to the intensive care unit, he had a temperature of 37.6 °C rectally, a pulse of 210 beats per minute and blood pressure of 78/48 mm Hg. He required ventilator and circulatory support. He was diagnosed with parechovirus infection“ (Watanabe et al., 2014).
Both Parechovirus and Enterovirus infection are associated with white matter brain injury. Dr Evans claims that air embolism can cause such injury, but he provides no credible evidence for this assertion. Given the combination of symptoms observed in the cluster of infants from Child G- J, it appears that the symptoms among the infants were similar because they exhibited clear neurological complications. In a case study of 6 neonates who survived parechovirus infection, distinctive supratentorial white matter and callosal diffusion abnormality were observed on MR imaging. The authors reported occipital (visual cortex) white matter and cortical involvement in 2/6 cases, which may relate to cases where visual issues have been described. It was additionally suggested that reported hypoglycaemia and transient hypoglycaemia or, alternatively, a seizure-related or vascular phenomenon, secondary to parechovirus infection, may be responsible for these neurological findings (Sarma et al., 2019). In fatal cases of parechovirus infection, it has been suggested that venous ischaemia causes white matter damage. A postmortem examination study of 2 premature neonates (33 and 34 weeks gestational age) with fatal HPeV infection by Bissel et al., demonstrated severe inflammatory changes of the periventricular white-matter with macrophage infiltration and astrocytosis. These findings are similar to those observed in hypoxic ischaemic encephalopathy due to birth complications.
It was stated that Child G was being fed breast milk, Gaviscon and formula. The article reports on three cases of gastric bezoar (a pathological conglomeration of foreign material found in the gastrointestinal tract) and one case of bowel obstruction. In a separate case, a 3-week-old female developed recurrent episodes of blood oxygen desaturations that were considered to be secondary to gastro-oesophageal reflux. Alginate–bicarbonate combination (Gaviscon®) was then added to her milk to prevent these events. She tolerated her feeds well and there were no abdominal symptoms apart from a full abdomen. However, her desaturations continued and 48 hours later, chest radiography was carried out to evaluate a possible respiratory cause. It was identified that the infant had developed a bezoar due to the combination of milk and Gaviscon. This case is relevant as it reveals that oxygen desaturations were unrelated to reflux as they persisted irrespective of the treatment provided. Again, there is no presentation of other risk factors which could ensure a physiological mechanism underpinning the symptoms observed in Child G. There are clear differences stemming from prematurity that were overlooked by Dr Evans, such as the fact that preterm infants have a lower capacity for the digestion of human milk (Demers-Mathieu et al., 2018). The role this might play in some of the gastric symptoms observed for Child G cannot be understated.
Projectile vomiting may reveal the beginning of a shift in the infant's overall presentation, which might explain the development of a condition called pyloric stenosis. There is a suggestion that pyloric stenosis is linked to poor innervation of nerves on the muscles in the gut, which cause the opening between the stomach and the intestines to thicken, preventing digested food from being able to pass through to the intestines (Macdessi and Oates, 1993). The blockage results in the forceful projection of food. An ultrasound or MRI would reveal a blockage. The reason the child's stomach was still full would be due to the fact that the stomach cannot empty. The vagus nerve extends from the brain stem to the gut and regulates gut movements. Recent evidence has shown that stimulation of the vagus nerve can permit gastric emptying in pyloric stenosis. The prematurity of the infant is a key factor here, and it appears the hospital failed to do sufficient brain scanning to ascertain the development of white brain matter, which is often impaired in premature infants. This should have been considered by the expert witnesses and properly evaluated given the that the conclusions they reached as to cause of death are exceedingly rare and are unsupported by the evidence.