Congenital syphilis is caused by the spirochete, Treponema pallidum, which can be transmitted from an infected mother to her fetus during pregnancy or by contact with a maternal lesion at the time of delivery. The incidence of congenital syphilis is rapidly increasing all over world with 700,000 to 1.5 million cases reported annually between 2016 and 2023. Despite the widespread availability of Penicillin, 2677 cases were reported in 2021 in the US. Clinical manifestations at birth can vary widely ranging from asymptomatic infection to stillbirth or neonatal death. Low birth weight, rash, hepatosplenomegaly, osteolytic bone lesions, pseudoparalysis, central nervous system infection, and long-term disabilities have been reported in newborns with congenital syphilis. Prevention of congenital syphilis is multifaceted and involves routine antenatal screening, timely treatment of perinatal syphilis with penicillin, partner tracing and treatment, and health education programs emphasizing safe sex practices and strategies to curb illicit drug use. Neonatal management includes risk stratification based on maternal syphilis history, evaluation (nontreponemal testing, complete blood counts, cerebrospinal fluid, and long-bone analysis), treatment with penicillin, and followup treponemal testing. Public health measures that enhance early detection during pregnancy and treatment with penicillin, especially in high-risk mothers, are urgently needed to prevent future cases of congenital syphilis.

Congenital syphilis (CS) has dramatically increased in the United States (US) in the past decade despite the widespread availability of penicillin. Once considered an infection on the verge of elimination, CS has re-emerged as a familiar neonatal pathogen in US hospitals. This rise in cases has prompted the evaluation of potential causes and updates in prevention and management guidelines. Following a structured narrative approach, we reviewed CS data reports, peer-reviewed research articles, and updated management guidelines from state health departments over the past two decades. Our main search criteria centered on the treatment and prevention of CS, with a focus on prenatal health disparities. We identified geographical regions reporting disproportionate rates of CS, examined state laws regarding maternal syphilis testing, and evaluated potential reasons for the recent rise in cases. This article examines the current epidemiology, screening, and management recommendations for perinatal and CS in the US. It also reviews pathogenesis and clinical features in perinatal and pediatric populations. Finally, it highlights the likely contributing factors to increased CS rates and identifies areas for future research. Dramatically rising CS cases in certain regions and racial groups reflect gaps in the prevention, timely diagnosis, treatment, and management of perinatal syphilis and CS. Healthcare providers attending to mothers and children should recognize the re-emergence of this pathogen and be familiar with new screening and management guidelines. Increased federal funding for targeted interventions and research that address vulnerable populations is critical to curbing the re-emergence of this infection.

Objectives Neonatal resuscitation guidelines recommend 0.5–1 mL saline flush following 0.01–0.03 mg/kg of epinephrine via low umbilical venous catheter for persistent bradycardia despite effective positive pressure ventilation (PPV) and chest compressions (CC). We evaluated the effects of 1 mL vs 3 mL/kg flush volumes and 0.01 vs 0.03 mg/kg doses on return of spontaneous circulation (ROSC) and epinephrine pharmacokinetics in lambs with cardiac arrest. Design Forty term lambs in cardiac arrest were randomised to receive 0.01 or 0.03 mg/kg epinephrine followed by 1 mL or 3 mL/kg flush after effective PPV and CC. Epinephrine (with 1 mL flush) was repeated every 3 min until ROSC or until 20 min. Haemodynamics, blood gases and plasma epinephrine concentrations were monitored. Results Ten lambs had ROSC before epinephrine administration and 2 died during instrumentation. Among 28 lambs that received epinephrine, 2/6 in 0.01 mg/kg-1 mL flush, 3/6 in 0.01 mg/kg-3 mL/kg flush, 5/7 in 0.03 mg/kg-1 mL flush and 9/9 in 0.03 mg/kg-3 mL/kg flush achieved ROSC (p=0.02). ROSC was five times faster with 0.03 mg/kg epinephrine compared with 0.01 mg/kg (adjusted HR (95% CI) 5.08 (1.7 to 15.25)) and three times faster with 3 mL/kg flush compared with 1 mL flush (3.5 (1.27 to 9.71)). Plasma epinephrine concentrations were higher with 0.01 mg/kg-3 mL/kg flush (adjusted geometric mean ratio 6.0 (1.4 to 25.7)), 0.03 mg/kg-1 mL flush (11.3 (2.1 to 60.3)) and 0.03 mg/kg-3 mL/kg flush (11.0 (2.2 to 55.3)) compared with 0.01 mg/kg-1 mL flush. Conclusions 0.03 mg/kg epinephrine dose with 3 mL/kg flush volume is associated with the highest ROSC rate, increases peak plasma epinephrine concentrations and hastens time to ROSC. Clinical trials evaluating optimal epinephrine dose and flush volume are warranted.

Hypoglycemia in neonates is associated with long-term neurodevelopmental effects. Hyperinsulinemic hypoglycemia (HH) is the most common cause of persistent hypoglycemia in neonatal intensive care units. Diazoxide is the only medication that is currently recommended for treatment of HH in neonates. However, the use of diazoxide in neonates is associated with pulmonary hypertension as an adverse effect. In this article, we review the literature on the mechanism of action and adverse effects with the use of diazoxide in neonatal hyperinsulinism. We then present a case series of neonates treated with diazoxide in our neonatal intensive care unit over a 5-year period. Among 23 neonates who received diazoxide, 4 developed pulmonary hypertension and 1 died. All infants who developed pulmonary hypertension were born preterm at less than 36 weeks gestation and had pre-existing risk factors for pulmonary hypertension. HH in preterm neonates, with pre-existing pulmonary hypertension or with risk factors for pulmonary hypertension requires thoughtful management.