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Introduction Disseminated neonatal herpes is one of the deadliest perinatal infections with a reported mortality of 85% in the untreated neonate with early commencement of aciclovir reducing this to 30%. Timely recognition is often difficult because of the non- specific presentation which delays the initiation of aciclovir. Case Series Report We report 3 cases of severe disseminated neonatal herpes (virology positive) seen in a year at our hospital with varying presentations and outcomes. Case 1: A baby (born at 36+6 weeks by caesarean section) presented on day 9 with lethargy and reduced feeding whereupon a septic screen was completed with commencement of intravenous antibiotics. On Day 10, the baby developed severe hyponatremia resistant to treatment and was therefore referred to a tertiary hospital at day 12 where he developed liver failure and disseminated intravascular coagulation (DIC). Despite aggressive management the baby died at day 25. Aciclovir was only started at day 14. Case 2: A 36+1 week baby born by caesarean section developed respiratory distress at day4 of life with rapid deterioration and chest X-ray changes. The baby was ventilated and transferred to a tertiary centre where he developed severe shock, liver failure and DIC. Aciclovir was started on day 5 but the baby succumbed and died on day 6. Case 3: A term baby born by normal vaginal delivery was admitted on day 9 with 2 day history of poor feeding, breathing difficulties and ulcer on the tongue. He was commenced on IV antibiotics and aciclovir. The bloods showed evidence of DIC and liver failure. The baby was transferred to a liver unit where he received intensive treatment for more than 1 month with gradual recovery following discharge. Discussion Disseminated neonatal herpes presents in varying scenarios often with symptoms starting between day 4–9. Of the three cases only one was commenced on aciclovir immediately on admission who eventually survived. Early commencement of aciclovir is crucial in neonates presenting with poor feeding, vesicular rash, severe hyponatremia, oral ulcers, seizures, bleeding etc. after 4 days of life.

Aims To identify obstacles to effective Kangaroo Mother Care (KMC) at a district hospital in rural Rwanda. Background KMC can improve thermoregulation and weight gain, whilst reducing infections and ultimately mortality. It can provide a safe alternative to incubator care for stable babies. Whilst KMC is often an established facility in Rwanda hospitals, local barriers may exist to limit the desired practice and outcomes in infants. Methods Over a 2-week period at the start of a 6-month placement, detailed observations of KMC practice 3 times a day were made. Results were collated and discussed with medical and nursing staff working in the neonatal unit. A programme to overcome key, local barriers to effective KMC was then devised. Results Key barriers and initiatives to overcome them were: Poor maternal nutrition – extreme local poverty and geographical isolation of the hospital on a mountain led to limited social support for mothers. Prolonged absence (and even absconding) of mothers was necessary to source food. Provision of a water filter and creation of a local egg cooperative helped to improve nutrition and minimise time needed away from their babies. With support for the cooperative from the adjacent church, free eggs are now provided daily to long–term mothers in the unit. Lack of space – a new, larger room for mothers undertaking KMC was sourced with our supervision, as part of a planned hospital re–organisation. This provided more space and independent washing facilities for mothers, creating a more pleasant environment. Lack of facilities –sourcing locally produced comfortable chairs and appropriate storage for belongings encouraged mothers to spend more effective time with their babies in KMC. Limited nursing staff – other members of the hospital staff, including social workers were mobilised to run education sessions on neonatal ‘red flags’ (i.e. fever, jaundice, lethargy, poor feeding). Basic educational materials and posters were provided to facilitate this. Conclusion Detailed observation followed by staff engagement allowed many of the obstacles to effective KMC to be overcome with low cost interventions. Nevertheless, innovative and local initiatives are critical to achieving major improvements.

Introduction Neonatal metabolic acidosis is a common presentation of wide range of causes varying from sepsis to rare metabolic and endocrine problems. Metabolic acidosis with normal anion gap help as to narrow down the cause as GI loss, RTA or adrenal insufficiency. We present a rare case of neonatal metabolic acidosis turned out to be due to adrenal insufficiency and subsequently diagnosed as SOD. Septo-optic dysplasia (SOD) is a rare congenital malformation syndrome characterised by a triad of optic nerve hypoplasia, midbrain abnormality and pituitary dysfunction. Case Report 19 day-old girl baby presented with lethargy, poor feeding and poor weight gain. On examination, she was hypothermic, hypoglycaemic, hyperkalaemia with early shock and metabolic acidosis. She was treated as presumed sepsis with dextrose, fluid bolus and antibiotics. She had persistent metabolic acidosis with normal anion gap despite on full feeds. Her septic screening and initial metabolic screening were negative. She was noted to have adrenal insufficiency (cortisol Conclusion Clinical followed by hormonal evaluation and imaging can guide us to its appropriate diagnosis and treatment of SOD. Early recognition of SOD is paramount in order to reduce morbidity and to optimise management. Without adequate treatment, panhypopituitism can have devastating effects on growth and neurodevelopment of children.

Background 6 month old baby, known case of Trisomy 21 with poor feeding. Case report A 6 month old baby girl was brought to emergency department by the mother as she was not feeding well for last few hours.Baby was born at term with an antenatal diagnosis of trisomy 21.She was exclusively breast fed since birth.Mom noticed an unusual appearance of a hard palate that she had not observed before.Her first impression was probably a cleft palate. On examination in emergency department baby was well looking ,alert with features of trisomy 21.Local examination of the palate revealed a piece of hazelnut that was stuck inside the hard palate.It was removed with the help of a spatulaunder direct visualisation in left lateral position.Baby was then discharged home as she was taking her feeds well. Discussion Foreign bodies of hard palate are rare.Most cases occur in infants.It can present in a variety of ways and most common is usual appearance mimicking oral pathology with poor feeding.Sometimes the diagnosis is challenging and there is always a choking hazard if there is delay in diagnosis.

Introduction Metabolic crisis in the neonatal period is an infrequently encountered, but potentially devastating presentation of an inborn error of metabolism. Due to the rarity of these disorders, diagnosis may be delayed. Furthermore, presentation may closely mimic neonatal sepsis, a much more frequently encountered condition. We describe the case of a neonate who presented at day nine with non-specific symptoms and signs. Careful evaluation of biochemical abnormalities led to a timely diagnosis of a rare, potentially life threatening metabolic disorder – Argininosuccinic Aciduria. Clinical Case A nine day old female infant presented with three days of poor feeding, lethargy and reduced urine output. Examination identified hypothermia (34.5C), tachypnoea, and a decreased level of consciousness. She was the first child of non-consanguineous Irish parents, with no family history of metabolic disorders. She was delivered at term by spontaneous vaginal delivery to non-consanguinous Irish parents, following an uncomplicated pregnancy. There were no septic risk factors or concerns at discharge on day 3. Blood glucose and inflammatory markers were normal. She was fluid resuscitated and commenced on broad-spectrum antibiotics. Despite treatment, she deteriorated. Venous blood gas showed respiratory alkalosis (pH 7.458, pCO2 3.92, HCO3 20.8, BE -2.4, lactate 1.0) prompting further investigation. Serum ammonia was 562. Retrospective review of investigations identified an unrecordable urea ( Conclusion Argininosuccinic aciduria is a rare, autosomal recessive disorder of urea cycle metabolism caused by deficiency of argininosuccinic lyase. Clinical and biochemical manifestations depend on the severity of enzyme deficiency. In the neonatal variant, it typically presents with hyperammonaemia, encephalopathy and respiratory alkalosis. This case highlights the importance of considering inborn errors of metabolism in the assessment of a sick neonate.

Background There is a national strategy ATAIN aimed at reducing term admissions to the neonatal unit. Whilst this is aimed at looking at potentially preventable term admissions to the neonatal unit, it does not address the issue of re-admission following discharge from the postnatal ward or neonatal unit. Given the limited midwifery resources in the community, we believe some of the re-admissions are potentially preventable if there were adequate resources to support the mother and baby at home. Aims To review the reasons for readmissions from home and identify potentially avoidable causes. Methods We retrospectively reviewed the BadgerNet neonatal electronic patient record to identify readmissions over the last financial year between 01/04/2017 and 31/03/2018. A standard excel profoma was used to collect and analyse the data. The reason for admission, interventions carried out and outcome was reviewed including the length of stay. Results In the last financial year there were 142 babies resulting in 143 readmissions to the postnatal or transitional care ward. Of these 120 babies were re-admitted for jaundice as a primary cause of admission. Of these jaundiced babies, 31 also had associated weight loss noted on admission. One baby had two episodes of re-admission for jaundice. Five of these babies had an infection screen, which were negative and antibiotics were discontinued by 48hrs. The median length of stay was 4 days and the range was between 3 and 11 days. Only one had admission to the neonatal unit with bronchiolitis. The total length of stay for the 120 babies was 446 days. Another 22 babies were readmitted because of weight loss. The median length of stay was 3 days and the range was between 1–4 days. The total length of stay for the 22 babies was 70 days. Of all the re-admission, 99 were breastfeeding on re-admission, 24 were mixed feeds and 19 bottle fed. Conclusions The two main reasons for readmissions were jaundice and weight loss. There was an overlap of this because a proportion of jaundiced babies were noted to have weight loss or poor feeding on readmission. We believe that these are potentially avoidable readmissions if there was sufficient feeding support for the mother and babies in the community. It would alleviate the additional emotional stress imposed on the mother and family by the readmission. It would also reduce the impact on the bed occupancy on an already stretched maternity and transitional care wards.

Aims To share our use of four-way communication between paediatric intensive care (PIC), tertiary neurology, parents and a district general hospital in an unusual situation. Method A male baby was born at 37 weeks weighing 2410 and had symmetrical IUGR. Initial tests did not reveal a cause. The baby was admitted to hospital twice because of poor feeding and poor weight gain. Aged 2 months he had marked hypotonia and was admitted for the second time. Echocardiogram showed left ventricular hypertrophy, serum lactate was elevated at 4.5 mmol/L (n 7.7 mmol/L, serum lactate had increased to 8.4 mmol/L. Leigh’s syndrome was strongly suspected but not definite. This is an inherited, usually mitochondrial, untreatable and terminal disorder. Due to impending respiratory failure a transfer to PICU was requested. A conference call initially involving the Consultant Paediatrician, Paediatric Neurologist and Paediatric Intensivist concluded that initiation of intensive care would inevitably lead to palliation in this case. We then invited parents to join the conference call who were able to ask the specialist questions directly and finally agree that intensive care was not in the best interests of their child. Results The baby was palliated in the DGH and died 24 hours later. 15 months later genetic tests confirmed novel heterozygous recessive mutations in a complex 1 gene as the cause of the Leigh syndrome. Conclusions We believe that use of technology to ensure clear communication in a complex situation was vital in achieving the appropriate outcome for our patient. This approach could easily be adopted wherever call conferencing is available.

Aim To discuss the case of a baby presenting with reversible progressive paralysis due to infantile botulism. Case This is the first case of infantile botulism in the UK since 2013 which presented after long haul travel to USA. A five month old girl with no history of illness presents with a rapidly progressing descending symmetrical paralysis. She had no significant past medical or familial history. Her initial complaint was difficulty in breast feeding followed by a rapid deterioration with hypotonia and respiratory failure. As a result, she was intubated and ventilated for 11 days whilst she was investigated extensively in paediatric intensive care. She was clinically thought to have infantile botulism and after a positive culture she was successfully treated with Baby BIG (immunoglobulin) for infantile botulism. She is back to her normal baseline. Investigations Initial blood tests and cerebrospinal fluid analysis including cell counts, protein and glucose were normal. Echocardiogram, electro-encephalogram and nerve conduction study were normal. Needle electromyography (EMG) found small, short and polyphasic motor unit action potentials. A PCR for detection of Clostridium botulinum type B neurotoxin genes in faecal specimens was negative. The mouse assay test was only partly positive and diagnosis was eventually confirmed by stool culture. Discussion Infantile botulism is an orphan disease that specifically affects infant less than 12 months of age. It is most commonly acquired in the United States with between 70–100 cases reported annually. In the UK it is a rare disease; there are now fourteen reported cases of infantile botulism in the UK. It is due to absorption of botulin toxin produced within the intestinal tract by temporary colonising clostridia. Infantile botulism typically presents with constipation and poor feeding. However, the clinical presentation may vary from mild hypotonia to severe bulbar paralysis and sudden infant death. It is a rare but important differential diagnosis in progressive hypotonia or paralysis in an infant in the UK. It has a completely reversible cause and effective treatment. As a result, this case highlights the importance of taking an accurate travel and diet history.

Objective To document the clinical features and management of infants presenting with fever after their first meningococcal B vaccination, and develop guidance for clinicians. Design A prospective case series over a 12 month period. Setting The Royal Hospital for Children Glasgow, a tertiary paediatric hospital. Patients Infants≤3 months of age who had received their first set of immunisations (including Bexsero) within the preceding 72 hours and reported fever. Results Ninety two infants met the inclusion criteria, accounting for 0.78% of the local vaccinated population. The most commonly described features were poor feeding, sleepiness and irritability. Sixty six patients (72%) were admitted to hospital. Median CRP was 12 mg/L and median WCC was 16 × 109/L.Fifteen patients (16%) had a lumbar puncture and were commenced on antibiotics. There was one confirmed bacterial infection in an infant who had presented with fever starting 54 hours after immunisation. All other microbiology samples were negative. There were no cases of missed serious bacterial infection (SBI) in those patients observed or discharged. Conclusion Post-immunisation fever is a common presenting problem to the paediatric emergency department. Based on our findings, routine investigations are not warranted if the infant appears well on examination. Where other common side effects are present and there is clinical concern, a period of observation may be a reasonable option. We suggest selective use of investigations, especially inflammatory markers, that are unlikely to discriminate between serious bacterial infection and post-immunisation response. We advocate extra caution in infants presenting with fever more than 48 hours after immunisation.

Introduction Bacterial dysentery represents an acute intestinal infection caused by an array of species of the Shigella genus, clinically characterised by the dysenteric syndrome – fever, abdominal pain, tenesmuses, bloody, mucoid diarrhoea and, which can sometimes complicate with systemic toxic manifestations. Material and method We present the case of a young child aged 1 year and 4 months admitted in the 9th Paediatric Department at The National Institute of Infectious Diseases „Prof. Dr. Matei Bals’ for fever, bloody, mucoid diarrhoea, vomiting, poor feeding, and one paroxysmal neurological manifestation associated with altered general status. Biological specimens were collected and immediate treatment was initiated – intravenous fluid therapy, antibiotic (Ceftriaxone), anticonvulsant and symptomatic treatment. Results Workup revealed leukocytosis with neutrophilia, important inflammatory syndrome, associated hepatic cytolysis and acid-base and hydro-electrolytic imbalances and positive stool cultures for Shigella sonnei were obtained after cultivation on specific media. The neurologic evaluation and EEG confirmed neurological involvement secondary to systemic shigellosis. Under treatment, the child’s general status improved, with subsequent normalisation of the stools and after seven days, the patient was cured and discharged in a normal general state, without any neurological sequelae and with negative stool cultures. Conclusion The presented case is an example of a toxic systemic form of shigellosis, with favourable evolution and complete clinical recovery, without sequelae but who requires subsequent neurological monitoring. Even though rarely encountered, the systemic severe form of paediatric dysentery can sometimes cause severe complications, sequelae and can lead to death in the absence of adequate treatment.