[Sudden infant death syndrome (SIDS)]. / La sindrome della morte improvvisa del lattante (SIDS).

Sudden Infant Death Syndrome (SIDS) is the term first proposed in 1969 for a distinctive subgroup of unexpected infant deaths occurring during the first months of life, with relatively consistent clinical, epidemiological and pathological features, which remain unexplained after a thorough case investigation, including a complete autopsy, examination of death scene and review of clinical history. Sudden infant death unnecessary means SIDS. According to definition, SIDS remains a diagnosis of exclusion, distinguished from others only by subjective and permissive variables. Despite the vague and permissive nature of the definition, epidemiological studies identified some risk factors as prematurity and social disadvantage. Nevertheless, the most interesting findings are those related to environmental and care features, as drug addiction and/or smoke exposition during pregnancy, sleep position of the infant, environmental temperature, parental bed sharing and breast feeding. Those factors play a variable role, but their correction reduced SIDS incidence. Sudden infant death is a diagnosis made by expert pathologists with pediatrician's and investigator's advice, based primarily on autopsy findings and death scene investigation performed through the severe application of investigative protocols.

Prolongation of the QT interval and the sudden infant death syndrome.

BACKGROUND: The sudden infant death syndrome (SIDS) is multifactorial in origin, but its causes remain unknown. We previously proposed that prolongation of the QT interval on the electrocardiogram, possibly resulting from a developmental abnormality in cardiac sympathetic innervation, may increase the risk of life-threatening ventricular arrhythmias and contribute to this devastating disorder. We prospectively tested this hypothesis. METHODS: Between 1976 and 1994, we recorded electrocardiograms on the third or fourth day of life in 34,442 newborns and followed them prospectively for one year. The QT interval was analyzed with and without correction for the heart rate. RESULTS: One-year follow-up data were available for 33,034 of the infants. There were 34 deaths, of which 24 were due to SIDS. The infants who died of SIDS had a longer corrected QT interval (QTc) than did the survivors (mean [+/-SD], 435+/-45 vs. 400+/-20 msec, P<0.01) and the infants who died from causes other than SIDS (393+/-24 msec, P<0.05). Moreover, 12 of the 24 SIDS victims but none of the other infants had a prolonged QTc (defined as a QTc greater than 440 msec). When the absolute QT interval was determined for similar cardiac-cycle lengths, it was found that 12 of the 24 infants who died of SIDS had a QT value exceeding the 97.5th percentile for the study group as a whole. The odds ratio for SIDS in infants with a prolonged QTc was 41.3 (95 percent confidence interval, 17.3 to 98.4). CONCLUSIONS: Prolongation of the QT interval in the first week of life is strongly associated with SIDS. Neonatal electrocardiographic screening may permit the early identification of a substantial percentage of infants at risk for SIDS, and the institution of preventive measures may therefore be possible.

QT interval prolongation and risk of life-threatening arrhythmias during toxoplasmosis prophylaxis with spiramycin in neonates.

We recently reported two cases of QT interval prolongation and cardiac arrest in newborns receiving antibiotic therapy with spiramycin, a macrolide agent extensively used for toxoplasmosis prophylaxis. In this study we assessed the effects of this drug on ventricular repolarization and on the potential risk of lethal arrhythmias in eight newborn infants in whom toxoplasmosis prophylaxis after birth was necessary. Electrocardiograms (ECGs) and echocardiograms were recorded during spiramycin therapy (350,000 i.u./kg/ day) and after its withdrawal. In a control group of eight healthy newborns matched for age and sex, no differences were found between two ECGs analogously recorded. The QT interval corrected for heart rate (QTc) was longer during spiramycin therapy than after drug withdrawal (448 +/- 32 msec vs 412 +/- 10 msec, +9%, p = 0.021). QTc dispersion, expressed as the difference between the longest and the shortest value in 12 different leads (QTcmax-min), was also higher during spiramycin therapy (60 +/- 32 msec vs 34 +/- 8 msec, +76%, p = 0.021), mainly because of a major lengthening of the longest QTc (QTcmax). QTc and QTc dispersion were markedly increased in the two newborns who experienced cardiac arrest after beginning treatment compared with the six neonates who had no drug-induced symptoms. During therapy seven of eight newborns had a rare abnormality in the thickening of the left ventricular posterior wall similar to that observed in patients with congenital long QT syndrome. This abnormality disappeared after drug withdrawal. Thus antibiotic therapy with spiramycin in the neonatal period may induce QT interval prolongation and increase QT dispersion. When this effect on ventricular repolarization is more marked, it may favor the occurrence of torsades des pointes and lead to cardiac arrest.

[Syncopal fainting episodes and gastroesophageal reflux]. / Episodi lipotimico sincopali e reflusso gastroesofageo.

Fainting syncopal events are caused by a transient functional neuronal paralysis. Reflex syncope happens for brainstem involving mediated by peripherical afferents. Sometimes gastroesophageal reflux (GER) has been implicated in the development of obstructive apnea. Gastroesophageal reflux, despite the absence of a clinical history of vomiting and regurgitation, is observed in a significant proportion of infants presenting with ALTE (Apparent Life Threatening Event): an episode characterized by some combination of apnea, color change, marked change in muscle tone, choking or gagging. Though a cause-and-effect relationship between GER and the development of ALTE remains to be established a possible direct relationship between oesophageal acidification and the onset of alterations in cardiopulmonary function and impairment of consciousness can be hypothesized. We refer the case of two female infants that developed recurrent ALTE(s) characterized by paleness, change in muscle tone and loss of consciousness. The infants resulted affected respectively by a mild and severe gastroesophageal reflux (score: 40, > 50); in one case an episode of GER was recorded by the intraoesophageal pH-monitoring during a syncopal episode. The treatment with antiacid drugs was effectual and the infants did not present ALTE(s). The cases presented are in favour of a routine search of gastroesophageal reflux in infants presenting with one or recurrent ALTE(s). The identification of these infants will permitt to develop a correct strategy of treatment.