Hypercapnea and Hypoxia Challenge Tests in Infants at Risk for Sudden Infant Death Syndrome

Lindenberg, Jeffrey A.; Newcomb, James D.

doi:10.1001/archpedi.1986.02140190076030

Cited by 2 publications

(1 citation statement)

References 18 publications

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“…45 Respiratory rate and pauses in response to a hypoxic challenge in 74 near-SIDS infants were not significantly different from those of 7 normal babies and 21 siblings of SIDS victims. 44 In summary, even normal infants do not respond predictably to hypoxia, and the hypoxic ventilatory responses in near-SIDS infants have been inconsistent.…”

Section: Ventilatory Responsiveness To Hypoxiamentioning

confidence: 98%

Are bedding and rebreathing suffocation a cause of SIDS?

Guntheroth

Spiers

1996

Pediatr. Pulmonol.

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Suffocation by bedclothes became a popular diagnosis in the 1940s but gradually became replaced with the diagnostic label of Sudden Infant Death Syndrome (SIDS). In 1991 a paper purported that, instead of SIDS, pillows filled with polystyrene beads had caused death by rebreathing suffocation; this conclusion was reached on the basis of experiments with anesthetized rabbits breathing through a doll's head that was placed face down on the pillow. Because of the anesthesia, rabbits could not change their face down position. The doll's nares could not collapse, which would have resulted in rapid death due to conventional suffocation. The rabbits required up to 3 hours or more to die of hypercarbia and hypoxia. Studies in normal infants revealed that they turned from the face‐down position after only 2 minutes. (The only infant who retained CO2 soon died of a fatal neurologic disorder, with central hypoventilation). Using the rabbit/doll's head and mechanical models, a wide range of bedding was indicted, including cushions, sheepskins, pillows, comforters, foam mattresses, and even simple blankets and sheets as potentially causing fatal rebreathing. Except for the use of pillows in general, as well as mattresses filled with kapok and bark, there has been no epidemiologic support for these indictments. Although normal infants are unlikely to succumb to rebreathing suffocation, infants with blunted ventilatory responsiveness and delayed arousal duo to prior hypoxia were hypothesized to be at increased risk. Support for this concept was found in the pathology of the brain stem in victims of SIDS that was attributed to prior hypoxic injury. In infants who survived prolonged apnea, less than 20% have demonstrated a diminished ventilatory responsiveness to hypercarbia, but, more significantly, none had an absent response. Arousal to hypercarbia, an abnormality which is crucial to the hypothesis of rebreathing suffocation, is regularly present in normal subjects, but the threshold is higher in near‐SIDS infants; however, no instances of failure to arouse have been reported in near‐SIDS. If the infant is placed on his or her back or side, the issue of bedding could become moot; unfortunately, a sizable percentage of infants are still being placed prone for sleep. Instead of confusing parents with an ever‐expanding list of “dangerous bedding,” the message “Back to Sleep” should be emphasized. Pediatr Pulmonol, 1996; 22:335–341. © 1996 Wiley‐Liss, Inc.

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Section: Ventilatory Responsiveness To Hypoxiamentioning

confidence: 98%

Are bedding and rebreathing suffocation a cause of SIDS?

Guntheroth

Spiers

1996

Pediatr. Pulmonol.

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Respiratory and arousal responses to hypoxia in apnoeic infants reinvestigated

et al. 1989

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Respiratory and arousal responses to mild hypoxia (15% oxygen in nitrogen) were recorded in 18 healthy infants and 33 infants who had sustained severe sleep related apnoeic events (ALTE). Respiratory movements and transcutaneous gas pressures (tcPO2 and tcPCO2) were continuously monitored during the 10 min test. The changes in tcPCO2 in relation to the decrease in tcPO2 were used as an index of the ventilatory and metabolic responses to hypoxia. We found that the response of apnoeic infants was within the range of the controls although the distribution of the individual response slopes was shifted towards the lower end of the range. Arousal was observed in 33% of apnoeic infants and 32% of the controls. Regular periodic breathing occurred in 42% of apnoeic infants compared to 28% of controls. In contrast to the controls, periodic breathing in apnoeic infants was not associated with a drop in tcPCO2 to below baseline levels. Apnoeic infants also alternated between regular and periodic breathing during the test. These findings are suggestive of a weak feed back control of breathing but do not support former views of a deficient hypoxic response in infants with ALTE.

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Hypercapnea and Hypoxia Challenge Tests in Infants at Risk for Sudden Infant Death Syndrome

Cited by 2 publications

References 18 publications

Are bedding and rebreathing suffocation a cause of SIDS?

Are bedding and rebreathing suffocation a cause of SIDS?

Respiratory and arousal responses to hypoxia in apnoeic infants reinvestigated

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