Carotid body in the sudden infant death syndrome.

Sixty-three percent of victims of the sudden infant death syndrome had a subnormal volume and 23 percent an enlarged volume of glomic cells in their carotid bodies. Evidences of antecedent chronic alveolar hypoxia and hypoxemia were found in both groups but were more severe in the victims with enlarged glomic tissue.

Hypoxemia and the sudden infant death syndrome.

Infants with known chronic hypoxemia before death retained a large proportion of the brown fat cells that are normally replaced by white fat cells after birth. Many of these hypoxemic infants also had an abnormal retention of extramedullary hematopoiesis. These same abnormalities were found in many victims of the sudden infant death syndrome.

Sudden infant death syndrome and subsequent pregnancy.

In psychological conditions of mourning and guilt, women who have lost children often attempt to quickly conceive a "replacement" child. This study examines the subsequent pregnancies of 32 women whose children died of sudden infant death syndrom (SIDS). The expected rate of infertility in a normal population is 10%. Spontaneous abortion has an incidence of 12% to 15%. Among the 32 women attempting to conceive after the loss of their child, 10 (31%) had spontaneous abortions and 11 (34%) could not conceive after attempts for at least one year. This association between psychological and biological phenomena require special recognition by physicians who are advising parents who have lost children to SIDS. The management of these families includes compassion, understanding, and regard for the psychological environment of the subsequent pregnancy.

Elevated levels of hypoxanthine in vitreous humor indicate prolonged cerebral hypoxia in victims of sudden infant death syndrome.

Hypoxanthine levels in vitreous humor from 32 infants who died of sudden infant death syndrome (SIDS) were determined and compared with levels found in eight children who died of trauma, drowning, or hanging and with levels from seven neonates dying suddenly without long-standing antemortem hypoxia. Determination of hypoxanthine level was done with either a PO2 electrode method or high-performance liquid chromatography. The results obtained by both methods were significantly correlated; therefore they were pooled. The median hypoxanthine level in victims of SIDS (380 mumol/L) was significantly higher (P less than .001) than in the children who died violently (118 mumol/L). Moreover, the levels from the SIDS victims were significantly higher (P less than .001) than those from the neonates who died without long-standing hypoxia (53 mumol/L). It is concluded that SIDS is probably not a sudden event but may be preceded by a relatively long period of respiratory failure and hypoxia.

Sudden infant death syndrome: hypothesis of causation.

The airway of the young infant is anatomically vulnerable at the oropharyngeal level between the soft palate and the base of the skull. Airway occlusion at this level might occur during the muscle relaxation which occurs during REM sleep, facilitated by a hypermobile mandible, by the hypotonia of infection, perhaps by an enlarged tongue with a strong backwards sucking action which might be the result of the artificial feeding of the infant. It is possible that "cot deaths" (SIDS) may be precipitated by such oropharyngeal airway occlusion, cardiac arrest following variable periods of partial or complete oxygen deprivation.

Brainstem auditory evoked responses in infants at risk of sudden infant death.

Brainstem auditory evoked responses (BAERs) were recorded from 63 near-miss Sudden Infant Death Syndrome (NMSIDS) infants, 26 siblings of SIDS (SSIBS) infants and 67 control infants between 0 and 30 weeks post-term. The majority of BAERs recorded from the NMSIDS and SSIBS infants had normal form and interpeak intervals (V-I and V-IIn) within normal limits for their age. However, 15% of these infants had interpeak intervals outside the normal range, suggesting abnormal neural function in these cases. The distributions of interpeak intervals for all NMSIDS and SSIBS infants were skewed towards longer times compared to control infants. The distributions of V-IIn intervals for both groups of at risk infants were significantly different to that of control infants. While the observations confirm that the recording of BAERs is not suitable for identifying infants at risk of SIDS, they suggest, however, that maturation of neural processing in the brainstem of these infants may be delayed.

Asbestos bodies in children's lungs. An association with sudden infant death syndrome and bronchopulmonary dysplasia.

Lungs from 46 autopsied children (age range, 1 to 27 months) were examined for asbestos bodies using a bleach-digestion extraction technique. Ten (21.7%) of 46 children had asbestos bodies in their lungs. Of these ten children, seven were diagnosed with sudden infant death syndrome, and three were diagnosed with bronchopulmonary dysplasia. Thus, 46.6% of children with sudden infant death syndrome and 42.8% of children with bronchopulmonary dysplasia had asbestos bodies. Impaired lung-clearing mechanisms due to either abnormal lung physiology or reorganization of pulmonary architecture may be significant in the formation of asbestos bodies. Additionally, children with asbestos bodies may have been exposed to higher ambient levels of asbestos and other pollutants.

Thal fundoplication: a simple and safe operative treatment for gastroesophageal reflux.

One hundred patients with complications of severe gastroesophageal reflux were treated surgically by the Thal fundoplication. In all patients the symptoms of reflux were eliminated by the operation, although 4 recurred within 8 months. Two of these were due to disruption of the fundoplication and two were due to hiatus hernia not recognized and repaired at initial operation. There were 8 deaths, none related to gastroesophageal reflux or the operation. Four patients required re-operation for intestinal obstruction. The Thal fundoplication is a simple procedure which fixes the distal esophagus within the abdomen and produces an acute angle of His. It is effective in prevention of reflux and the patient is able to burp and vomit if necessary. It has not been associated with dysphagia or "gas bloat" which may follow the Nissen fundoplication.

Sudden infant death syndrome associated with rotavirus infection.

Rotavirus was detected in the stools of five children stricken with sudden infant death syndrome (SIDS) over a three-week period. While none of the children had acute gastroenteritis, four of the five had acute upper respiratory infections. Rotavirus was also identified in tracheal aspirates from two of the infants. Extensive investigations failed to reveal the presence of any other viruses or toxins in specimens obtained from the five children with SIDS. Rotavirus was not found in the stool specimens obtained from a control group of 36 infants including six who died of causes other than SIDS. Future attempts at the prevention of rotavirus infections should be directed at populations susceptible to sudden infant death syndrome.

Defects of metabolism of fatty acids in the sudden infant death syndrome.

Two hundred consecutive cases of the sudden infant death syndrome were reviewed for the presence of fat in the liver; 14 showed diffuse panlobular microvesicular fatty change indistinguishable from that found in Reye's syndrome. Samples of frozen liver were available in five of the 14 cases; histochemical analysis showed well preserved cytochrome oxidase and succinate dehydrogenase activity in all five, uncharacteristic of Reye's syndrome. Fatty acyl-coenzyme A dehydrogenase activity in the liver was assayed biochemically in two of the same five cases with severe hepatic fatty infiltration; both showed a defect in medium chain acyl-coenzyme A dehydrogenase activity using the substrate octanoyl-coenzyme A. Both cases also showed cerebral oedema in association with fatty infiltration of renal tubules, myocardium, and skeletal muscle, characteristic of Reye's syndrome. It is concluded that diffuse panlobular microvesicular fatty change of the liver in victims of the sudden infant death syndrome, although essentially non-specific, indicates that the state of mitochondrial enzymes should be investigated.

Serological evidence of recent influenza virus A (H 3 N 2) infections in forensic cases of the sudden infant death syndrome (SIDS).

40 forensic SIDS cases were found to have a significantly higher rate of serologic evidence of recent influenza A (H 3 N 2) infection than did matched controls. In contrast, the SIDS cases had serologically no significantly increased infection rate with influenza H 1 N 1 and B virus, parainfluenza virus, RS virus, adenovirus, and cytomegalovirus. SIDS cases with recent influenza infection had a significantly higher rate of histological findings as described for primary viral pneumonia than did SIDS cases without influenza infection. SIDS cases with recent influenza infection occurred much more frequently during epidemic than during interepidemic influenza A (H 3 N 2) periods. Our results confirm previous reports that SIDS cases have an increased rate of respiratory virus infections. However, they cannot prove a causal relationship between influenza infection and death. Since our SIDS cases comprised 75 per cent of cases aged more than three months, our results pertain essentially to cases of this age group.