Fetal alcohol spectrum disorder (FASD) is a set of conditions resulting from prenatal alcohol exposure (PAE). FASD is estimated to affect between 2% and 5% of people in the United States and Western Europe. The exact teratogenic mechanism of alcohol on fetal development is still unclear. Ethanol (EtOH) contributes to the malfunctioning of the neurological system in children exposed in utero by decreasing glutathione peroxidase action, with an increase in the production of reactive oxygen species (ROS), which causes oxidative stress. We report a case of a mother with declared alcohol abuse and cigarette smoking during pregnancy. By analyzing the ethyl glucuronide (EtG, a metabolite of alcohol) and the nicotine/cotinine in the mother’s hair and meconium, we confirmed the alcohol and smoking abuse magnitude. We also found that the mother during pregnancy was a cocaine abuser. As a result, her newborn was diagnosed with fetal alcohol syndrome (FAS). At the time of the delivery, the mother, but not the newborn, had an elevation in oxidative stress. However, the infant, a few days later, displayed marked potentiation in oxidative stress. The clinical complexity of the events involving the infant was presented and discussed, underlining also the importance that for cases of FASD, it is crucial to have more intensive hospital monitoring and controls during the initial days.

Neurological complications in pregnancy and the puerperium deserve particular attention from specialists due to the worsening of the clinical picture for both the mother and the fetus. This narrative review of existing data in the literature aims to analyze the most common “red flag symptoms” attributable to neurological complications such as pre-eclampsia (PE), eclampsia, HELLP syndrome, posterior reversible encephalopathy syndrome (PRES), cerebral vasoconstriction syndrome (RCVS), stroke, CVS thrombosis, pituitary apoplexy, amniotic fluid embolism and cerebral aneurysm rupture, with the aim of providing a rapid diagnostic algorithm useful for the early diagnosis and treatment of these complications. The data were derived through the use of PubMed. The results and conclusions of our review are that neurological complications of a vascular nature in pregnancy and the puerperium are conditions that are often difficult to diagnose and manage clinically. For the obstetrics specialist who is faced with these situations, it is always important to have a guide in mind in order to be able to unravel the difficulties of clinical reasoning and promptly arrive at a diagnostic hypothesis.

Prenatal alcohol exposure is responsible for increasing chronic disease risk in later life, including obesity and metabolic syndrome. Alcohol drinking may compromise endogenous antioxidant capacity, causing an increase in free radicals and reactive oxygen species in the newborn. Excessive reactive oxygen species could attack the cellular proteins, lipids, and nucleic acids, leading to cellular dysfunction. Moreover, oxidative stress could play a crucial role in the altered synthesis and release of neurotrophins and progressive mitochondrial modifications with uncontrolled apoptosis. This narrative review aims to underline the important role of alcohol abuse in oxidative stress events and consequent metabolic and neurocognitive impairments in children exposed to alcohol during gestational life.