The following is an overview of the Sudden Infant Death Syndrome (SIDS) and emphasizes salient features of its epidemiology, pathology, pathophysiology and management. Controversial points are not discussed

Marsland, David W.

VCU Scholars Compass

The Nature of the Problem: Sudden Infant Death Syndrome DAVID W. M ARSLAND, M.D. Professor o f Family Practice and Associate Professor of Pediatrics, Medical College of Virginia , Health Sciences Division of Virginia Commonwealth University, Richmond, Virginia The following is an overview of the Sud-den Infant Death Syndrome (SIDS) and em-phasizes salient features of its epidemiology, pathology, pathophysiology and management. Controversial points are not discussed. Epidemiology SIDS is an increasingly common problem with a reported incidence of 2 to 3 per 1 , 000 live births. In the United States, there are ap-proximately 1 0 ,000 deaths per year. For Vir-ginia in 1976, there were 129 reported cases. In the 1 972 King County, Washington study, from one week to 11 months of age the leading cause of death is SIDS (45%), followed by congenital malformations (20%). From one week to 1 4 years of age SIDS is the third lead-ing specific cause of death behind diseases of early infancy and accidents. SIDS is more com-mon in males than females, 3: 2. The syndrome is more common in the economically dis-advantaged, with blacks having an incidence of 5 per 1 ,000 live births. Infants of lower birth weight and gestational age have a higher in-cidence of the problem For example the risk for babies weighing 3 lbs s ·oz is 13.27 per 1 ,000 live births. Paradoxically, infants who weighed This is an edited transcript of the remarks by Dr. Marsland at the Sudden Infant Death Syndrome Sym-posium held June 1, 1979, at the Richmond Hyatt House, Richmond, Virginia. Correspondence and reprint requests to Dr. David W. Marsland, Box 251, Medical College of Virginia, Rich-mond, VA 23298. less than 3 lbs 8 oz at birth have a decreasing incidence, but the lower incidence may reflect the high mortality from respiratory disease in the neonatal period. SIDS is most common at 2 to 4 months of life with few cases being reported be-fore 2 weeks and after 1 2 months. Nasophar-yngitis seems to accompany SIDS. In the north-ern hemisphere, SIDS tends to occur more frequently in winter; whereas in the southern hemisphere, the syndrome occurs more com-monly in summer months. About 7 4% of all deaths are discovered during sleep in the early morning hours. It should be remarked that nationally, there is considerable debate as to the true epidemiology of SIDS. Pathology During the past ten years pathologists have assisted in bringing about a better un-derstanding of the syndrome. SIDS is defined as , ''The sudden death of any infant or young child, which is unexpected by history, and in which a thorough postmortem exam fails to demonstrate an adequate cause of death.''* By definition an autopsy is then nec-essary to rule out SIDS. Beckwith reported a series of 500 au-topsies in infants dying during the first year of life. In 1 5% a cause of death could be found (infection , trauma, major malformations and others) . In 87% of the infants intrathoracic • J. B. Beckwith: " The Sudden Infant Death Syn-drome. " Pediatrics 3 29, 1973. MCV QUARTERLY 15(4)11 5-116, 1980 / 115 petechiae were noted. A number of observa-tions by investigators from pathological speci-mens would tend to indicate that infants dying of SIDS are chronically hypoxemic . These findings would include leukomalacia, demyelinization of the brain , intrathoracic pe-techiae , decreased cytoplasmic granules in carotid chemoreceptors, increased muscle mass in the small pulmonary arterioles, extra-medullary hematopoiesis and retention of brown fat. Other autopsy findings in SIDS would include normal nutrition and hydration, perhaps some blood-tinged sputum or frothy fluid at the mouth or nostrils, diapers wet or full of stool, clutched hands, pulmonary con-gestion or edema, perhaps some interstitial pulmonary lymphocytic infiltrate, normal size adrenal glands, normal thymus and no evi-dence of aspiration. Pathophysiology Why do babies die of SIDS? What is a near-miss SIDS and how does it relate to SIDS? How does the physician identify the in-fant at risk for SIDS? Answers to these ques-tions would be important to the child and the clinician. As yet there are no clear answers but many clues. A near-miss infant is defined as a pre-viously well infant who, during sleep, experi-enced an episode of apnea, limpness, cy-an osi s o r pallor that was terminated by vigorous stimulation or mouth-to-mouth resusci-tation. It has now been documented that a number of infants with near-miss SIDS die of SIDS. These near-miss infants need the follow-ing : 1) complete physical and neurological examination , 2) complete blood count, 3) urinal-ysis , 4) serum ca++, P04 - , Mg++, glu-cose, Na+, K+ and amino acids, 5) capillary blood gases , 6) urine organic and amino acids, 7) chest and skull x-ray, 8) barium swallow, 9) 1 2-lead electrocardiogram, and 1 0) sleep and awake electroencephalogram . Included in the differential diagnoses are sei-zures, esophagopharyngeal reflux , sepsis and aspiration. The control of ventilation is a very deli-cately balanced system. The near-miss SIDS and SIDS victim would appear to have abnor-mal control of ventilation especially during sleep. Study of ventilation in the small infant is diffi-cult and not available except in research lab-11 6 / MARSLAND: PROBLEMS OF SIDS oratories. Sleep and awake electroencephalo-grams, ventilatory response to various inspired gas mixtures and thoracic and nasal movements are monitored in an integrated system. To date it has been demonstrated that the near-miss SIDS infant has hypoventila-tion , a depressed ventilatory response to C02 breathing , prolonged sleep apnea, frequent short apnea, periodic breathing and apnea clus-tered in sleep. Apnea in near-miss infants has been demonstrated in REM and Quiet Sleep. In addition to evidence for abnormal control of ventilation during sleep clinical in-vestigations have hypothesized that obstruc-tive apnea may occur during the terminal event. Tonkin demonstrated the anatomic vul-nerability at the oropharyngeal level between the soft palate and the base of the skull in the small infant. In REM sleep with muscle re-laxation this anatomic vulnerability may lead to oropharyngeal occlusion. In near-miss SIDS infants abnormalities of muscle tone have been demonstrated particularly shoulder hypotonia. In one case study, loss of electromyogram (EMG) activity of the genioglossus muscle with obstructive sleep apnea has been confirmed . Several family members had died from SIDS. Therefore, the near-miss SIDS and SIDS patient would appear to have chronic hypoxe-mia, abnormal control of venti lation during sleep and possibly an obstructive asphyxia! event. Despite all of the evidence, the patho-physiology is not completely explained and a simple test to identify the infant at risk has not been forthcoming. Management Autopsies should be performed on all in-f ants who are thought to have SIDS. The postmortem will rule out abuse and infanticide and other diagnoses. The parents can then with certainty be told that their infant died from SIDS and that they could not have pre-vented the death . A common denominator for the family is guilt which when combined with grief and lack of knowledge can lead to major emo-tional stress, exacerbation of previous psychi-atric conditions, and marital problems. To al-leviate the guilt and grief the parents should be referred to a SIDS guild, and should be helped by many counseling visits to their pe-diatrician or family physician. 

The Nature of the Problem: Sudden Infant Death Syndrome

http://scholarscompass.vcu.edu/cgi/viewcontent.cgi?article=1606&context=mcvq

The Nature of the Problem: Sudden Infant Death Syndrome

Abstract

Similar works

Full text

Available Versions

VCU Scholars Compass