Guía de la Sociedad Española de Infectología Pediátrica sobre tuberculosis en la embarazada y el recién nacido (I): epidemiología y diagnóstico. Tuberculosis congénita / Spanish Society for Pediatric Infectious Diseases guidelines on tuberculosis in pregnant women and neonates (i): Epidemiology and diagnosis. Congenital tuberculosis

El cribado de tuberculosis (TB) gestacional mediante la realización de la prueba de tuberculina (PT) se recomienda a las embarazadas con síntomas compatibles, contacto íntimo con TB bacilífera o riesgo de progresión a formas activas. Las nuevas técnicas de diagnóstico interferon gamma release assay (IGRA) están indicadas en gestantes sin factores de riesgo, con PT positiva y antecedente de vacunación BCG, y en inmunodeprimidas con sospecha clínica y PT negativa. El diagnóstico de enfermedad es difícil, ya que los síntomas pueden ser inespecíficos y hay más formas extrapulmonares, por el retraso en las exploraciones radiológicas y por la mayor tasa de anergia a la tuberculina. La TB neonatal puede adquirirse de forma intrauterina (TB congénita) o por vía respiratoria tras el parto (TB posnatal). La TB congénita es excepcional, no produce malformaciones fetales y, aunque puede estar presente en el nacimiento, suele iniciarse a partir de la segunda semana de vida. En ausencia de antecedentes familiares, la TB neonatal debe sospecharse en caso de neumonía con patrón miliar, hepatoesplenomegalia con lesiones focales o meningitis linfocitaria con hipoglucorraquia, especialmente si la madre procede de áreas de alta endemia de TB. La PT es habitualmente negativa y la sensibilidad de los IGRA es inferior a la de niños de más edad. Sin embargo, la baciloscopia y el cultivo de jugo gástrico tienen una rentabilidad superior, especialmente en la TB congénita. Las técnicas de diagnóstico molecular permiten un diagnóstico precoz y la detección de mutaciones de resistencia farmacológica. El riesgo de formas diseminadas y la mortalidad son elevados

Tuberculosis (TB) screening in pregnancy using tuberculin skin test (TST) is recommended in case of symptoms of TB disease, close contact with a patient with infectious TB, or high risk of developing active disease. The new interferon gamma release assay (IGRA) tests are recommended in BCG-vaccinated pregnant women with positive TST and no known risk factors for TB, and in those immunocompromised, with clinical suspicion of TB but negative TST. TB diagnosis is difficult due to the non-specific symptoms, the increased frequency of extrapulmonary disease, the delay in radiological examinations, and the high rate of tuberculin anergy. Neonatal TB can be acquired in utero (congenital TB), or through airborne transmission after delivery (postnatal TB). Congenital TB is extremely rare and does not cause fetal malformations. It may be evident at birth, although it usually presents after the second week of life. In newborns with no family history of TB, the disease should be considered in cases of miliary pneumonia, hepatosplenomegaly with focal lesions, or lymphocytic meningitis with hypoglycorrhachia, especially in those born to immigrants from high TB-burden countries. TST is usually negative, and IGRAs have lower sensitivity than in older children. However, the yield of acid-fast smear and culture is higher, mostly in congenital TB. Molecular diagnosis techniques enable early diagnosis and detection of drug resistance mutations. There is a substantial risk of disseminated disease and death

Guía de la Sociedad Española de Infectología Pediátrica sobre tuberculosis en la embarazada y el recién nacido (II): profilaxis y tratamiento / Spanish Society for Pediatric Infectious Diseases guidelines on tuberculosis in pregnant women and neonates (II): Prophylaxis and treatment

En la embarazada expuesta a tuberculosis (TB) no se recomienda profilaxis primaria con isoniazida salvo en gestantes inmunodeprimidas, con enfermedades crónicas o factores de riesgo obstétrico y antecedente de contacto íntimo mantenido con un enfermo bacilífero. En la infección tuberculosa latente (ITBL) se iniciará profilaxis con isoniazida si existe contacto reciente con TB o factores de riesgo de progresión a TB activa. En caso contrario, se retrasará hasta al menos 3 semanas después del parto. El tratamiento de la enfermedad tuberculosa es el mismo que fuera de la gestación. Los recién nacidos de madres con historia gestacional de TB diseminada o extrapulmonar, con TB activa en el parto o con contacto TB posnatal conocido, asintomáticos y con pruebas diagnósticas negativas, deben recibir profilaxis primaria con isoniazida durante al menos 12 semanas. Transcurrido ese tiempo se repiten los test diagnósticos, y si son negativos, se interrumpe la profilaxis. En la ITBL, se administrará isoniazida durante 9 meses. En la enfermedad tuberculosa, el tratamiento es el mismo que en el niño mayor pero mantenido al menos 9 meses. Se recomienda aislamiento respiratorio en la TB congénita y en la TB posnatal con baciloscopia positiva en jugo gástrico o aspirado bronquial. La separación madre-hijo solo está indicada en madres que han recibido tratamiento durante menos de 2 semanas, presentan baciloscopia positiva o tienen TB resistente. La lactancia materna no está contraindicada y en las situaciones de separación la madre puede extraerse la leche para que sea administrada en biberón al recién nacido

In pregnant women who have been exposed to tuberculosis (TB), primary isoniazid prophylaxis is only recommended in cases of immunosuppression, chronic medical conditions or obstetric risk factors, and close and sustained contact with a patient with infectious TB. Isoniazid prophylaxis for latent tuberculosis infection (LTBI) is recommended in women who have close contact with an infectious TB patient or have risk factors for progression to active disease. Otherwise, it should be delayed until at least three weeks after delivery. Treatment of TB disease during pregnancy is the same as for the general adult population. Infants born to mothers with disseminated or extrapulmonary TB in pregnancy, with active TB at delivery, or with postnatal exposure to TB, should undergo a complete diagnostic evaluation. Primary isoniazid prophylaxis for at least 12 weeks is recommended for those with negative diagnostic tests and no evidence of disease. Repeated negative diagnostic tests are mandatory before interrupting prophylaxis. Isoniazid for 9 months is recommended in LTBI. Treatment of neonatal TB disease is similar to that of older children, but should be maintained for at least 9 months. Respiratory isolation is recommended in congenital TB, and in postnatal TB with positive gastric or bronchial aspirate acid-fast smears. Separation of mother and infant is only necessary when the mother has received treatment for less than 2 weeks, is sputum smear-positive, or has drug-resistant TB. Breastfeeding is not contraindicated, and in case of mother-infant separation expressed breast milk feeding is recommended

[Spanish Society for Pediatric Infectious Diseases guidelines on tuberculosis in pregnant women and neonates (i): Epidemiology and diagnosis. Congenital tuberculosis]. / Guía de la Sociedad Española de Infectología Pediátrica sobre tuberculosis en la embarazada y el recién nacido (I): epidemiología y diagnóstico. Tuberculosis congénita.

Tuberculosis (TB) screening in pregnancy using tuberculin skin test (TST) is recommended in case of symptoms of TB disease, close contact with a patient with infectious TB, or high risk of developing active disease. The new interferon gamma release assay (IGRA) tests are recommended in BCG-vaccinated pregnant women with positive TST and no known risk factors for TB, and in those immunocompromised, with clinical suspicion of TB but negative TST. TB diagnosis is difficult due to the non-specific symptoms, the increased frequency of extrapulmonary disease, the delay in radiological examinations, and the high rate of tuberculin anergy. Neonatal TB can be acquired in utero (congenital TB), or through airborne transmission after delivery (postnatal TB). Congenital TB is extremely rare and does not cause fetal malformations. It may be evident at birth, although it usually presents after the second week of life. In newborns with no family history of TB, the disease should be considered in cases of miliary pneumonia, hepatosplenomegaly with focal lesions, or lymphocytic meningitis with hypoglycorrhachia, especially in those born to immigrants from high TB-burden countries. TST is usually negative, and IGRAs have lower sensitivity than in older children. However, the yield of acid-fast smear and culture is higher, mostly in congenital TB. Molecular diagnosis techniques enable early diagnosis and detection of drug resistance mutations. There is a substantial risk of disseminated disease and death.

[Spanish Society for Pediatric Infectious Diseases guidelines on tuberculosis in pregnant women and neonates (ii): Prophylaxis and treatment]. / Guía de la Sociedad Española de Infectología Pediátrica sobre tuberculosis en la embarazada y el recién nacido (ii): profilaxis y tratamiento.

In pregnant women who have been exposed to tuberculosis (TB), primary isoniazid prophylaxis is only recommended in cases of immunosuppression, chronic medical conditions or obstetric risk factors, and close and sustained contact with a patient with infectious TB. Isoniazid prophylaxis for latent tuberculosis infection (LTBI) is recommended in women who have close contact with an infectious TB patient or have risk factors for progression to active disease. Otherwise, it should be delayed until at least three weeks after delivery. Treatment of TB disease during pregnancy is the same as for the general adult population. Infants born to mothers with disseminated or extrapulmonary TB in pregnancy, with active TB at delivery, or with postnatal exposure to TB, should undergo a complete diagnostic evaluation. Primary isoniazid prophylaxis for at least 12 weeks is recommended for those with negative diagnostic tests and no evidence of disease. Repeated negative diagnostic tests are mandatory before interrupting prophylaxis. Isoniazid for 9 months is recommended in LTBI. Treatment of neonatal TB disease is similar to that of older children, but should be maintained for at least 9 months. Respiratory isolation is recommended in congenital TB, and in postnatal TB with positive gastric or bronchial aspirate acid-fast smears. Separation of mother and infant is only necessary when the mother has received treatment for less than 2 weeks, is sputum smear-positive, or has drug-resistant TB. Breastfeeding is not contraindicated, and in case of mother-infant separation expressed breast milk feeding is recommended.

Guía de la Sociedad Española de Infectología Pediátrica para el diagnóstico y tratamiento de la toxoplasmosis congénita / The Spanish Society of Pediatric Infectious Diseases Guidelines for the diagnosis and treatment of congenital toxoplasmosis

La toxoplasmosis congénita es la consecuencia de la transmisión fetal por vía transplacentaria de Toxoplasma gondii tras la primoinfección materna. El riesgo de infección fetal es bajo en infecciones en el primer trimestre y va aumentando con la edad gestacional, mientras que la gravedad de la infección disminuye con esta. El diagnóstico de infección materna se realiza mediante la demostración de seroconversión o ante la presencia de IgM positiva con anticuerpos IgG de baja avidez. Las gestantes con infección demostrada deben recibir espiramicina para intentar evitar su transmisión al feto. El diagnóstico de infección fetal se realiza mediante reacción en cadena de la polimerasa (PCR) en líquido amniótico obtenido a partir de la semana 18 de gestación. Si esta prueba resulta positiva, debe iniciarse tratamiento a la embarazada con pirimetamina, sulfadiazina y ácido folínico. La mayoría de los niños infectados nacen asintomáticos pero hasta el 80% desarrolla secuelas visuales o neurológicas durante su infancia y adolescencia. El diagnóstico neonatal es complicado porque los anticuerpos IgM e IgA y la PCR en sangre y líquido cefalorraquídeo pueden ser falsamente negativos. En estos casos, el diagnóstico puede realizarse mediante la constatación de un ascenso significativo de los anticuerpos IgG o la persistencia de los mismos después del año de vida. El tratamiento neonatal con pirimetamina y sulfadiazina disminuye la posibilidad de secuelas a largo plazo. La toxoplasmosis congénita es una enfermedad prevenible mediante el cribado pregestacional y la adopción de medidas de profilaxis primaria en las gestantes seronegativas (AU)

Congenital toxoplasmosis is the result of transplacental fetal infection by Toxoplasma gondii after the primary maternal infection. The severity of the disease depends on the gestational age at transmission. First trimester infections are more severe, but less frequent, than third trimester infections. Acute maternal infection is diagnosed by seroconversion or by the detection of IgM antibodies and a low IgG avidity test. In these cases, spiramycin should be initiated to prevent transmission to the fetus. For identification of fetal infection, polymerase chain reaction (PCR) testing of amniotic fluid after 18 weeks gestation should be performed. If fetal infection is confirmed, the mothers should be treated with pyrimethamine, sulfadiazine and folinic acid. Most infants infected in utero are born with no obvious signs of toxoplasmosis, but up to 80% developed learning and visual disabilities later in life. Neonatal diagnosis with IgM/IgA antibodies or blood/cerebrospinal fluid PCR may be difficult because false-negative results frequently occur. In these cases diagnosis is possible by demonstrating a rise in IgG titers during follow-up or by the detection of antibodies beyond one year of age. Early treatment with pyrimethamine and sulfadiazine may improve the ophthalmologic and neurological outcome. Congenital toxoplasmosis is a preventable disease. Pre-pregnancy screening and appropriate counseling regarding prevention measures in seronegative women may prevent fetal infection (AU)

[The Spanish Society of Pediatric Infectious Diseases Guidelines for the diagnosis and treatment of congenital toxoplasmosis]. / Guía de la Sociedad Española de Infectología Pediátrica para el diagnóstico y tratamiento de la toxoplasmosis congénita.

Congenital toxoplasmosis is the result of transplacental fetal infection by Toxoplasma gondii after the primary maternal infection. The severity of the disease depends on the gestational age at transmission. First trimester infections are more severe, but less frequent, than third trimester infections. Acute maternal infection is diagnosed by seroconversion or by the detection of IgM antibodies and a low IgG avidity test. In these cases, spiramycin should be initiated to prevent transmission to the fetus. For identification of fetal infection, polymerase chain reaction (PCR) testing of amniotic fluid after 18 weeks gestation should be performed. If fetal infection is confirmed, the mothers should be treated with pyrimethamine, sulfadiazine and folinic acid. Most infants infected in utero are born with no obvious signs of toxoplasmosis, but up to 80% developed learning and visual disabilities later in life. Neonatal diagnosis with IgM/IgA antibodies or blood/cerebrospinal fluid PCR may be difficult because false-negative results frequently occur. In these cases diagnosis is possible by demonstrating a rise in IgG titers during follow-up or by the detection of antibodies beyond one year of age. Early treatment with pyrimethamine and sulfadiazine may improve the ophthalmologic and neurological outcome. Congenital toxoplasmosis is a preventable disease. Pre-pregnancy screening and appropriate counseling regarding prevention measures in seronegative women may prevent fetal infection.

[Neonatal convulsions and subarachnoid hemorrhage after in utero exposure to paroxetine]. / Convulsiones y hemorragia subaracnoidea tras exposición a paroxetina in utero.

INTRODUCTION: Selective serotonin reuptake inhibitors (SSRIs) are often used as antidepressants in pregnant women. SSRIs do not appear to increase the teratogenic risk when used in their recommended doses. However, not enough information is available at this time about the risk of toxicity and complications in newborns, after mother treatment with SSRI during the third trimester of pregnancy. We are limited to the existing reports that describe newborns with symptoms due to hyperserotoninemia or withdrawal. CASE REPORT: One newborn whose mother had been treated with paroxetine 20 mg/day during pregnancy, presented convulsions and subarachnoid haemorrhage in the first six hours of life. The newborn did not present symptoms of hypoxic ischaemic encephalopathy, withdrawal syndrome, infection, metabolic alterations, cerebral malformations or coagulopaties. DISCUSSION: The most probable etiology is that the paroxetine could decrease the seizure threshold, taking place the first seizure during delivery. The difficult fetal extraction would have provoked the subarachnoid haemorrhage in a patient with an impaired haemostatic function due to a depletion of platelet serotonin and may also contribute the increased vascular fragility due to paroxetine and reported in adults or in animals. CONCLUSION: Neonatal convulsions and subarachnoid haemorrhage may occur after paroxetine treatment in the third trimester of pregnancy. An accurate follow up of these newborns in the firsts days of life is strongly recommended.

Convulsiones y hemorragia subaracnoidea tras exposición a paroxetina in utero / Neonatal convulsions and subarachnoid hemorrhage after in utero exposure to paroxetine

Introducción. Los inhibidores selectivos de la recaptación de serotonina (ISRS) se emplean con frecuencia como antidepresivos en las mujeres embarazadas. Cuando se administran con la posología recomendada los ISRS no parecen aumentar el riesgo teratógeno. Sin embargo, actualmente no se dispone de suficiente información sobre el riesgo de producirse toxicidad y complicaciones en los neonatos después de tratarse la madre con ISRS durante el tercer trimestre de gestación. Sólo disponemos de los casos publicados donde se describen a neonatos con síntomas provocados por una hiperserotoninemia o por privación. Caso clínico. Un neonato, cuya madre se había tratado con 20 mg/día de paroxetina durante el embarazo, presenta convulsiones y una hemorragia subaracnoidea durante las seis primeras horas de vida. El neonato no presentaba síntomas de encefalopatía isquémica hipóxica, síndrome de abstinencia ,infección, trastornos metabólicos, malformaciones cerebrales ni coagulopatías. Discusión. La etiología más probable es que la paroxetina provoca una reducción del umbral convulsivo, las primeras convulsiones ocurriendo durante el parto. La difícil extracción del feto habría provocado una hemorragia subaracnoidea en un paciente con una disfunción hemostática causada por una disminución de la serotonina de los trombocitos y también puede contribuir al incremento de la fragilidad vascular ocasionada por la paroxetina que se ha descrito en los adultos o los animales. Conclusión. Las convulsiones y la hemorragia subaracnoidea pueden presentarse en los neonatos después de tratarse la madre con paroxetina durante el tercer trimestre del embarazo. Es muy aconsejable realizar un seguimiento exhaustivo de estos neonatos durante los primeros días de vida (AU)

Introduction. Selective serotonin reuptake inhibitors (SSRIs) are often used as antidepressants in pregnant women. SSRIs do not appear to increase the teratogenic risk when used in their recommended doses. However, not enough information is available at this time about the risk of toxicity and complications in newborns, after mother treatment with SSRI during the third trimester of pregnancy. We are limited to the existing reports that describe newborns with symptoms due to hyperserotoninemia or withdrawal.Case report. One newborn whose mother had been treated with paroxetine 20 mg/day during pregnancy, presented convulsions and subarachnoid haemorrhage in the first six hours of life. The newborn did not present symptoms of hypoxic ischaemic encephalopathy, withdrawal syndrome, infection, metabolic alterations, cerebral malformations or coagulopaties. Discussion.The most probable etiology is that the paroxetine could decrease the seizure threshold, taking place the first seizure during delivery. The difficult fetal extraction would have provoked the subarachnoid haemorrhage in a patient with an impaired haemostatic function due to a depletion of platelet serotonin and may also contribute the increased vascular fragility due to paroxetine and reported in adults or in animals. Conclusion. Neonatal convulsions and subarachnoid haemorrhage may occur after paroxetine treatment in the third trimester of pregnancy. An accurate follow-up of these newborns in the firsts days of life is strongly recommended (AU)

[Severe neonatal encephalopathy, secondary to a prolonged vasovagal episode in a woman 31 weeks pregnant]. / Encefalopatía neonatal grave, secundaria a episodio vasovagal prolongado en una gestante de 31 semanas.

INTRODUCTION: Vasovagal syncope is not frequent during the second half of pregnancy, although the supine hypotension syndrome is common during this period. During these episodes, the marked hypotension may impede uteroplacental blood flow. CASE REPORT: A woman who was 31.5 weeks pregnant lost consciousness for 15 minutes on standing up. 24 hours later, when it was observed that foetal movement had diminished, a cardiotocographic recording was done. This showed a pathological pattern and foetal biophysical profile on echography showed a marked foetal hypotonia and absence of movement. Emergency caesarean section was carried out and a male foetus delivered, weighing 1.810 g, with an Apgar score of 5/6 and requiring intubation and mechanical ventilation for respiratory difficulties and generalized hyptonia with absent reflexes. During the following days he developed generalized hypertonia and died aged 18 days. At necropsy there was severe brain damage, of ischaemic type. Complementary tests on the mother were normal. CONCLUSIONS: Severe prenatal encephalopathy secondary to maternal vasovagal syncope is uncommon, and we have found no report of it in the literature. The prolonged duration of the hypotensive episode, together with prematurity, which implies poor regulation of cerebral blood flow, may have contributed to the severe damage to the central nervous system

Encefalopatía neonatal grave, secundaria a episodio vasovagal prolongado en una gestante de 31 semanas / Severe neonatal encephalopathy, secondary to a prolonged vasovagal episode in a woman 31 weeks pregnant

Introducción. El síncope vasovagal es poco frecuente en la segunda mitad de la gestación, aunque en este período resulta frecuente el síndrome de hipotensión supina. En estos episodios, la hipotensión marcada puede dificultar el flujo uteroplacentario. Caso clínico. Gestante de 31,5 semanas que presenta pérdida de conciencia de 15 minutos al adoptar la bipedestación. A las 24 horas, al percibir disminución de movimientos fetales, se practica registro cardiotocográfico, que evidencia patrón patológico y perfil biofísico fetal, mediante ecografía, en el cual se observa hipotonía fetal marcada y ausencia de movimientos. Se practica cesárea urgente y se produce nacimiento de feto, varón de 1.810 g, Apgar 5/6 que requiere intubación y ventilación por dificultad respiratoria y con hipotonía generalizada con ausencia de reflejos. En los días siguientes desarrolla hipertonía de base y fallece a los 18 días de vida. En la necropsia se observa lesión encefálica grave de tipo isquémico. Exploraciones complementarias maternas, negativas. Conclusión. La encefalopatía prenatal grave secundaria a síncope vasovagal materno es una entidad muy poco frecuente, de la cual no hemos encontrado otros casos en la literatura. La prolongada duración del episodio hipotensivo, junto con la prematuridad que comporta escasa regulación del flujo cerebral, pudieron contribuir a la gran afectación del sistema nervioso central (AU)