Fetal complications of maternal heroin addiction: Abnormal growth, infections, and episodes of stress

Naeye, Richard L.; Blanc, William A.; Leblanc, Werner; Khatamee, M.

doi:10.1016/s0022-3476(73)80550-5

Cited by 177 publications

(49 citation statements)

References 23 publications

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“…[15][16][17][18] The use of illicit drugs like heroin and cocaine and exposure to various medications, such as warfarin, anticonvulsants, antineoplastic agents can result in FGR. [19][20][21] Maternal disease and systemic conditions such as reduced uteroplacental blood flow, reduced oxygen-carrying capacity, or decreased nutrition to the fetus, chronic hypertension, preeclampsia, pregestational diabetes, chronic renal insufficiency, systemic lupus erythematous (SLE), antiphospholipid syndrome, renal diseases, autoimmune diseases and acquired thrombophilia, chronic maternal hypoxemia due to pulmonary disease, cardiac disease have been associated with FGR. [22][23][24][25] maternal malnutrition, protein deficiency and gastrointestinal conditions can cause lower birth weight because of decreased nutrition to the foetus.…”

Section: Maternal Factorsmentioning

confidence: 99%

Fetal growth restriction: aetiology, screening, diagnosis and management

Augusthy

2015

Int J Reprod Contracept Obstet Gynecol

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Foetal growth restriction (FGR) is a pathological condition that refers to a foetus that fails to reach his/her genetically predetermined growth potential. FGR remains a leading contributor to perinatal mortality and morbidity and metabolic syndrome in later life. The purpose of this review is to provide the summary statements of the aetiology of FGR and to establish a framework for screening, diagnosis, and management of pregnancies affected with foetal growth restriction. For this study, published literature was retrieved through searches of PubMed (Medline), Highwire, Google Scholar, Scopus, Cochrane Database of Systematic Reviews. Conference/Seminar proceedings, textbooks, previously published systematic reviews, controlled clinical trials, high quality prospective and retrospective observational studies, research articles and unpublished studies were also used for this study. The identification of FGR begins with assessment of maternal, foetal, placental and environmental risk factors and the diagnosis is made by Ultrasound biometry examination. Functional assessment of placental and foetal circulation by Doppler velocimetry and blood flow volume, together with computerized assessment of foetal heart rate variability, are key examinations in early and late FGR to assess severity of the disease and monitor foetal wellbeing. Appropriate timing of delivery in early FGR might change the outcome, and appropriate monitoring in late and term FGR might avoid unnecessary interventions.

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Section: Maternal Factorsmentioning

confidence: 99%

Fetal growth restriction: aetiology, screening, diagnosis and management

Augusthy

2015

Int J Reprod Contracept Obstet Gynecol

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“…Naeye et al (10) in 1973, compared at autopsy infants born to heroin-addicted mothers to those infants born to a nonaddicted control group. The infants born following intrauterine narcotic exposure were SGA and had small placentas.…”

Section: Discussionmentioning

confidence: 99%

Fetal Growth Retardation following Maternal Morphine Administration: Nutritional or Drug Effect?

Raye¹,

Dubin²,

Blechner³

1977

Neonatology

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The effects of maternal morphine administration on maternal nutrition and on fetal growth have been systematically examined in a rabbit model. Significant alterations in maternal food intake occurred during morphine exposure. These nutritional changes did not result in fetal growth retardation. Fetal morphine exposure was associated with significant reductions in fetal weight, length, placental weight and in the weights of most organs including the brain. When organ weight was considered as a fraction of total fetal weight morphine exposure was associated with a significant increase in the relative weight of the brain and a significant decrease in the relative weight of liver and kidneys. These narcotic effects were dose dependent.

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“…Antenatal opiate exposure affects brain development 9,10 with resulting decreases in corticogenesis, neurogenesis, and synaptogenesis 11,12 and alterations in the ontogeny of the stress axis [13][14][15] and immune response. 16 Human studies also allude to the association of prenatal opiate exposure and small head circumference [17][18][19][20] and decreased brain volumes found on imaging. 21 An additional concern is that infants with NAS receive their pharmacologic treatment during the first few months of life, a period of rapid postnatal brain development.…”

Section: What's Known On This Subjectmentioning

confidence: 99%

Morphine Versus Clonidine for Neonatal Abstinence Syndrome

Bada¹,

Sithisarn²,

Gibson

et al. 2015

Pediatrics

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OBJECTIVE: The study goal was to determine whether clonidine treatment of neonatal abstinence syndrome (NAS) would result in a better neurobehavioral performance compared with morphine.METHODS: This pilot study prospectively enrolled infants $35 weeks' gestational age admitted for treatment of NAS. After informed consent was obtained, infants were randomized to receive morphine (0.4 mg/kg per day) or clonidine (5 mg/kg per day) divided into 8 doses. A 25% dose escalation every 24 hours was possible per protocol (maximum of 1 mg/kg per day for morphine and 12 mg/kg per day for clonidine). After control of symptoms, the dose was tapered by 10% every other day. Clinical staff monitored infants by using Finnegan scoring. Masked research staff administered the NICU Network Neurobehavioral Scale (NNNS) at 1 week and at 2 to 4 weeks after initiation of treatment and the Bayley Scales III, and Preschool Language Scale IV, at 1-year adjusted age. Analyses included descriptive statistics, repeated measures analysis of variance, and Wilcoxon tests.RESULTS: Infants treated with morphine (n = 15) versus clonidine (n = 16) did not differ in birth weight or age at treatment. Treatment duration was significantly longer for morphine (median 39 days) than for clonidine (median 28 days; P = .02). NNNS summary scores improved significantly with clonidine but not with morphine. On subsequent assessment, those receiving clonidine had lower height of arousal and excitability (P , .05). One-year motor, cognitive, and language scores did not differ between groups.CONCLUSIONS: Clonidine may be a favorable alternative to morphine as a single-drug therapy for NAS. A multicenter randomized trial is warranted. WHAT'S KNOWN ON THIS SUBJECT:Increased central adrenergic activity occurs with opiate withdrawal. Clonidine is an effective drug as an adjunct to morphine in the treatment of neonatal abstinence syndrome. It is unclear whether clonidine is effective as single-drug therapy.WHAT THIS STUDY ADDS: Clonidine, a a 2 -adrenergic agonist, seems to be as effective as morphine when used as a single-drug therapy for neonatal abstinence syndrome. Its administration results in improvement in neurobehavioral performance.

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Fetal complications of maternal heroin addiction: Abnormal growth, infections, and episodes of stress

Cited by 177 publications

References 23 publications

Fetal growth restriction: aetiology, screening, diagnosis and management

Fetal growth restriction: aetiology, screening, diagnosis and management

Fetal Growth Retardation following Maternal Morphine Administration: Nutritional or Drug Effect?

Morphine Versus Clonidine for Neonatal Abstinence Syndrome

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