Cases reported "Sudden Infant Death"

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1/16. Failure of mouth-to-mouth resuscitation in cases of sudden infant death.

    We describe two cases of sudden infant death syndrome (SIDS) and one case of apparent life threatening apnoea where resuscitation was attempted by the mouth-to-mouth route. This was associated with evidence of gastric distension, including reflux of milk into the airway in the first two cases. In the second case the mother used mouth-to-mouth breathing after finding that she could not cover her baby's nose-and-open-mouth with her mouth. In the last case, the mother went on to try the mouth-to-nose route, with a good outcome. Systematic documentation of the route of resuscitation and its outcome in all cases of SIDS and near-miss SIDS may provide valuable insights into the optimal route for infant resuscitation.
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2/16. sudden infant death syndrome and hypertrophy of the palatine tonsil: reports on two cases.

    Two cases of sudden infant death syndrome (SIDS) with hypertrophy of the palatine tonsil were reported. The pathogenesis of the SIDS has been clarified (Guilleminault et al., pediatrics, 68 (1981) 354-360). According to this theory, it is due to a central impairment of the breathing control during sleep, which is particularly pronounced in predisposed subjects. The present cases suggest that the hypertrophied palatine tonsil might contribute as a predisposing factor to the emergence of a SIDS by mechanical impediment to breathing by narrowing of the upper airway.
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3/16. sudden infant death: lingual thyroglossal duct cyst versus environmental factors.

    An 8-month-old female baby was found collapsed in the prone position 30 min after being positioned under soft-bedding. She was taken to the emergency room with cardiopulmonary arrest. Her heartbeat was recovered after resuscitation and continued for 20 h under artificial respiration, at which point the child died. At autopsy, the child showed no significant pathological abnormalities apart from a thyroglossal duct cyst of 2.0 cm diameter, therefore, it seemed that the cyst, which was close to the epiglottis, had caused asphyxia through airways occlusion. However, the child had shown no respiratory problems before death, and the risk of airway occlusion as a result of lingual cysts is more likely in a supine rather than a prone position. A small amount of evidence suggested that the child died as a result of suffocation from being covered by soft-bedding, which could have caused fatal asphyxia; it is also possible that a hypoxic state induced by airway obstruction might have been enhanced by being covered with bedding. It seemed reasonable to assume that death was caused by a combination of the lingual thyroglossal duct cysts and asphyxia caused by being covered in bedding, though the main factor appeared to be the large cyst.
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4/16. Dysphagia as a risk factor for sudden unexplained death in infancy.

    The TRIAD of encephalopathy, subdural haemorrhages, and retinal haemorrhages is commonly considered diagnostic of shaken baby syndrome, but the original paper describes a statistically linked QUADRAD of features, the fourth of which is a previous history of feeding difficulties (dysphagia). Recent reviews of giving pacifiers (dummies) to infants during sleeping periods have found a significant reduction in the incidence of sudden infant death Syndrome. Stimulation of swallowing is a possible connection with dysphagia, which is examined here, illustrated by a well documented case. Although amniotic fluid passes freely through the larynx of fetal mammals during fetal breathing, application of pure water to the laryngeal epithelium in infants causes choking and laryngeal closure. "water sensors" in the surface respond to lack of chloride ions and adapt very slowly or not at all. Others have found in puppies that following application of pure water only 32% resume breathing in less than 30-40s. The rest needed at least one saline flush, and some required artificial ventilation in addition. These receptors also respond to high potassium concentrations and acid or alkaline solutions. Normally, airway closure during swallowing or vomiting prevents entry of feed or oesophageal reflux, but in some forms of dysphagia leakage can occur, causing paroxysmal coughing, reflex laryngeal closure, and so prolonged apnoea. Recently, it has been realised that the TRIAD injuries can also result from high intracranial vascular pressures transmitted from intra-thoracic pressure surges during paroxysmal coughing, choking, etc. Triggering of such pressure surges by dysphagic accidents provides a physiological link to injuries commonly considered diagnostic of shaken baby syndrome, completing the statistically identified QUADRAD of features. Further dysphagic research might reveal predictive factors, and preventative measures such as feeds of optimal pH.
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5/16. Sudden and unexpected death between 1 and 5 years.

    Of a population of 9856 children followed up from birth, 9251 of whom underwent 24 hour tape recordings of electrocardiograms and abdominal wall breathing movements during early infancy, five died suddenly and unexpectedly at home at ages ranging from 16 months to 4 years. Postmortem examination, including full histological and microbiological investigations. failed to identify abnormalities ordinarily associated with death in all five cases. Two of the children were known to have had frequent cyanotic episodes and died during these events. In the three remaining cases there was no previous history of cyanotic or apnoeic episodes. The death of one of these three children was seen by his parents and the clinical features suggested that apnoea rather than a cardiac arrhythmia was the primary mechanism for his death. As in infancy, sudden and unexpected death for which no adequate cause is found at necropsy seems to constitute a major component of mortality between 1 and 5 years.
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6/16. ischemia of the brain stem as a cause of sudden infant death syndrome.

    Recent evidence indicates that the sudden infant death syndrome (SIDS) is related to abnormal control of respiration. Focal morphologic changes have not been noted. In a case of SIDS, ischemic degeneration was noted bilaterally in the medulla, particularly in the dorsal motor nucleus of the vagus nerve. Pathologic changes were not found elsewhere in the CNS. To our knowledge, this is the first description of a focal brain-stem lesion in SIDS that had enough of a role in altered respiratory control to cause death.
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7/16. A case of near-miss SIDS developing an abnormal respiratory reaction to hypoxia.

    A SIDS sibling is described who showed a normal respiratory regulation at 1.5 months but who was equipped with an apnea monitor at home on psychological indications. At 3 months he had a near-miss SIDS episode. He was then found to have developed a reaction to hypoxia with appearance of periodic breathing. With theophylline this response pattern was normalized but despite theophylline medication episodes of prolonged apnea occurred.
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8/16. REM sleep prevents sudden infant death syndrome.

    Near-miss events were observed to occur in indeterminate sleep in a preterm infant reaching term at 6 weeks after birth. Moreover, prolonged sleep apnea and periodic respiration were frequently encountered in non-REM sleep. In view of the observation that pathologic sleep apnea occurs in non-REM sleep and the apparently contradictory findings of respiratory depression and more frequent apneas during REM sleep, apneic episodes during REM sleep were analysed in relation to phasic REM events. The frequent occurrence of respiratory pauses in REM burst-free periods of REM sleep suggests that tonic REM mechanisms inhibit respiratory neurons, while phasic REM mechanisms are facilitatory and protect an infant from prolonged sleep apnea.
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keywords = respiration
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9/16. Respiratory and cardiac events observed and recorded during and following a "near miss" for sudden infant death Syndrome episode.

    Documented observations of a 5-week-old infant during a "near miss" for a Sudden Infant Death Syndrome (SIDS) episode by a physician were carried out during an in-hospital physiological recording of respiratory and cardiac activity. This "near miss" event occurred during quiet sleep and was characterized by a prolonged apneic attack with marked bradycardia, cyanosis and limpness which required immediate vigorous resuscitative efforts by a physician and trained nurse. Parental descriptions of similar events parallel these documented sudden unexpected changes in cardiorespiratory parameters. Objective polygraphic data were obtained immediately following the episode and at later ages during 24 and 48 hour continuous recordings of respiration, heart rate, sleep/wake and behavioral activity. The data show that numerous apneic episodes occurred following the "near miss" event, many accompanied by marked bradycardia. The moderately severe hypoxemia noted during these sleep-related apneas indicate that immediate intervention is required to prevent significant hypoxia and central depression in such infants.
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10/16. Epileptic seizure-induced hypoxemia in infants with apparent life-threatening events.

    OBJECTIVE. To describe the physiologic changes that occur during epileptic seizure (ES)-induced apparent life-threatening events (ALTE) and to provide an explanation for the mechanism whereby the hypoxemia characterizing these events occurred. patients AND DESIGN. Six infants were retrospectively selected from a group of 17 because they had ALTE documented on physiologic recordings where the first change in signals was in the electroencephalogram (EEG). The 17 infants had clinical features suggestive of partial seizures (but normal standard EEGs) and were from a sample of 172 infants with recurrent ALTE. All 17 infants underwent continuous recordings of breathing, electrocardiogram (ECG), oxygenation, and EEG, but only in 6 was an ES-induced ALTE recorded and the physiologic changes described. RESULTS. Twenty-three ALTE were documented in six infants. Events commenced with an abnormality in the EEG, followed by a decrease in SaO2 after a median interval of 27 seconds (range 2 to 147). Despite resuscitation, the median duration of severe hypoxemia (SaO2 < or = 60%) was 40 seconds (range 8 to 74). In 18 events (five infants) there was a median of four apneic pauses (range 1 to 9) preceding the decrease in SaO2 by a median duration of 24 seconds (range 3 to 48). The longest apneic pause per event lasted a median of 19 seconds (range 8 to 47). Breathing movements continued in five events (four infants), and expiratory airflow in one. Sinus tachycardia was found in 19 of the 23 events (six infants), but there were no cardiac arrhythmias. CONCLUSIONS. ES in infants can manifest as ALTE and be accompanied by potentially life-threatening episodes of severe hypoxemia and apnea, despite a normal EEG between events.
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