синдром внезапной смерти у новорожденных

[Andru]

Уважаемые неонатологи помогите разобраться с "Синдромом внезапной смерти". Есть ли такой диагноз или нет? Есть ли патанатомические признаки, может ли патанатом спутать с механической асфиксией например?

[Dr.Nathalie]

Pediatrics, Sudden Infant Death Syndrome
Last Updated: February 20, 2006 Synonyms and related keywords: SIDS, crib death, cot death, sudden infant death syndrome, prolonged QT interval hypothesis, apnea hypothesis, sudden unexpected death in infancy, SUDI
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Background: The National Institute of Child Health and Human Development defines sudden infant death syndrome (SIDS) as follows:

The sudden death of an infant under 1 year of age that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and a review of the clinical history.

The sudden demise of an infant, thankfully, is not a common occurrence. While the unexpected death of an infant may result from a number of processes, the leading cause is a syndrome with an etiology that has not been fully elucidated.
The diagnosis of SIDS is one of exclusion and, thus, should be demystified, with the specific evidence in each infant death subject to careful and complete examination.
In its Policy on Distinguishing Sudden Infant Death Syndrome from Child Abuse Fatalities, the Committee on Child Abuse and Neglect of the American Academy of Pediatrics states that the death of an infant may be attributed to SIDS when all of the following are true:

• A complete autopsy is performed, including cranium and cranial contents, and autopsy findings are compatible with SIDS;
• no gross or microscopic evidence of trauma or significant disease process is present;
• no evidence of trauma exists on skeletal survey;
• other causes of death are adequately ruled out, including meningitis, sepsis, aspiration, pneumonia, myocarditis, abdominal trauma, dehydration, fluid and electrolyte imbalance, significant congenital lesions, inborn metabolic disorders, carbon monoxide asphyxia, drowning, or burns;
• no evidence of current alcohol, drug, or toxic exposure is present;
• and thorough death scene investigation and review of the clinical history are negative.

Although death from SIDS is much more common than death from child abuse, the possibility of homicide, nevertheless, is an omnipresent etiologic overlay. Presentation of an infant with a life-threatening event creates many unique challenges for emergency physicians and has a high potential for producing cognitive dissonance.
Elicitation of the history of present illness, vital to every workup, may reveal inconsistencies that raise suspicions for human agency as the underlying cause of the infant's condition. Physical examination directed toward the identification of medical problems may reveal evidence of intentional trauma.
Treatment of physiologic instability must be conducted simultaneously with attention to identification and preservation of potential physical evidence. Even emotional support of the parents, integral to comprehensive medical management and compassionate medical practice, should be performed in a manner that does not compromise possible subsequent legal proceedings.
Informing parents of the death of a child is cited as the most stressful experience physicians confront in emergency medicine. These events often are compounded by feelings of guilt and inadequacy, which are experienced by most emergency physicians following an unsuccessful pediatric resuscitation. These reactions may be markedly different, qualitatively and quantitatively, from the emotions generally experienced by emergency physicians when confronting other crises.

Pathophysiology: This section begins with a discussion of the triple-risk model of SIDS, followed by specific examination of each of the proposed elements. A synthesis of these theories concludes the section.
Although multiple hypotheses have been proposed as the pathophysiologic mechanisms responsible for SIDS, none have been proven. The triple-risk model of SIDS proposes that the cause of SIDS is multifactorial and that the sudden death of an infant may occur when a predisposed infant is in an unstable period of homeostatic control and is exposed to triggering factors.
Prolonged QT interval hypothesis
QTc prolongation of more than 440 milliseconds, is a marker of reduced cardiac electrical stability and is strongly associated with SIDS. According to conservative estimates, 30-35% of infants who subsequently die of SIDS have prolongation of the QT interval in the first week of life.
The QTc increases during the second month of life but returns to values recorded at birth by the sixth month. These findings are derived from a large prospective study of infants born over a 19-year period and another study, which together examined more than 40,000 infants. The odds ratio for SIDS among all infants with prolonged QTc was 41:1; for boys, the odds ratio was approximately 47:1.
Developmental alteration in cardiac sympathetic innervation is one hypothesis proposed to explain QT prolongation. Such innervation continues after birth until an infant is approximately 6 months old. Occasionally, the right and left sympathetic nerves develop at different rates, creating a temporary neural imbalance. During this developmental stage, a sudden increase in sympathetic activity may cause a lethal arrhythmia in these electrically unstable hearts. This is most commonly torsade de pointes ventricular tachycardia due to early after-depolarizations.
A second hypothesis proposes a variant of the congenital long QT syndrome. Patients with this syndrome are at high risk for sudden death, especially under conditions of stress but also during sleep.
Prolongation of the QTc may act as an arrhythmogenic substrate that requires other postnatal factors to trigger development of life-threatening arrhythmias. The trigger is usually a sudden increase in sympathetic activity, which, during the first year of life, may have a number of causes, including sudden noise, apnea leading to a chemoreceptive reflex, exposure to cold, and rapid eye movement (REM) sleep and arousal.
Although the authors of these studies indicate that other traditional SIDS risk factors (eg, prone sleeping position, maternal smoking, bed sharing) have odds ratios markedly lower than that observed with QT prolongation, the American Academy of Pediatrics states it is unlikely that this irregularity explains more than a small minority of SIDS cases.

[Dr.Nathalie]

Apnea hypothesis
Terms used throughout this chapter are defined below, together with a differential list for some conditions. These definitions are based upon those promulgated by

• Apparent life-threatening event (ALTE): This is a frightening episode to observe. ALTE is characterized by some combination of apnea (central, occasionally obstructive), color change (usually cyanotic or pallid, occasionally erythematous or plethoric), marked change in muscle tone (usually limpness), choking, or gagging. In some cases, observers fear the infant has died. Survivors of an ALTE share many risk factors for SIDS and are at a statistically increased risk for the syndrome; however, debate exists as to whether ALTEs are interrupted SIDS events, separate phenomena, or events related to SIDS.
• Periodic breathing: This is a breathing pattern in which 3 or more respiratory pauses of more than 3 seconds duration are separated by less than 20 seconds of respiration between pauses. This breathing pattern can be normal.
• Pathologic apnea: A respiratory pause is abnormal if it is prolonged (>20 seconds) or associated with cyanosis; abrupt, marked pallor; hypotonia; or bradycardia.
• Apnea of prematurity: This type of apnea is characterized by periodic breathing with pathologic apnea in a premature infant. Apnea of prematurity usually ceases by 37 weeks' gestation (menstrual dating) but, occasionally, persists for several weeks past term.
• Apnea of infancy: This type of apnea is characterized by an unexplained episode of cessation of breathing for 20 seconds or more or a briefer respiratory pause associated with cyanosis, pallor, marked hypotonia, or bradycardia. This term generally refers to infants who are older than 37 weeks' gestational age at onset of pathologic apnea. These infants' ALTEs were idiopathic but were considered to be related to apnea. Accordingly, reserve apnea of infancy classification for those infants for whom no specific ALTE cause can be identified.

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[Dr.Nathalie]

Several anatomic and physiologic findings support the role of apnea in SIDS. SIDS, despite the apparent contradiction, is not always sudden. Meny et al reviewed data from 6 infants who died while on home monitors. Of these deaths, 3 were ascribed to SIDS. All SIDS patients had a bradycardia that preceded (2 cases) or occurred simultaneously with (1 case) central apnea. One of the patients had tachycardia prior to bradycardia. The monitor printout of 1 patient showed a slow decrease in heart rate for approximately 2 hours prior to death. One infant who had rapid cardiopulmonary resuscitation (CPR) could not be revived, suggesting that myocardial depression secondary to hypoxemia may have preceded the bradycardia.
Other evidence also suggests hypoxia (acute and chronic) as causal of SIDS. Hypoxanthine, a marker for tissue hypoxia, is elevated in the vitreous humor of patients who die from SIDS compared to controls who die suddenly. This evidence adds biochemical support to the concept that, in some patients, SIDS is a relatively slow process. In addition, a substantial number of infants who die from SIDS manifest necropathologic evidence of chronic hypoxia, including changes in the bronchiolar walls, pulmonary neuroendocrine cells in the lungs, and elevated fetal hemoglobin levels.
Alveolar hypoxia stimulates pulmonary vasoconstriction and, eventually, pulmonary vascular smooth muscle cell hyperplasia. Muscularity of the pulmonary vasculature causes pulmonary vasoconstriction, increased right ventricular afterload, and heart failure with more tissue hypoxia. Arterial hypoxemia and ischemia result in astrogliosis of the brainstem, which promotes hypoventilation and further astrogliosis.
Another significant autopsy finding is pleural petechiae, whose formation reflects acute hypoxia in a physiologically intact infant. Hypoxic asphyxia in newborns occurs in the following well-defined stages:

• Stage 1 - Tachypnea for 60-90 seconds followed by apparent loss of consciousness, passage of urine, and no respiratory effort
• Stage II - Deep, gasping respiratory efforts separated by 10-second periods of respiratory silence
• Stage III - Formation of pleural petechiae ultimately resulting in the cessation of gasping
• Stage IV - Death if resuscitation is not initiated

The latter stages of asphyxia are triggered when PaO2 falls toward zero. Asphyxia may occur with the airway open, partially occluded, or closed.
Although a significant number of SIDS autopsies do not demonstrate any pathological findings, most infants who die of SIDS have an extremely large number of petechiae. Their presence suggests that repeated episodes of asphyxia occurred in a period of hours to days prior to death, causing recurrent episodes of gasping with associated petechiae formation. Studies in newborn animals have shown that it takes hours to recover metabolically from asphyxia. Repeated episodes of asphyxia that were previously self-limited by arousal and autoresuscitation, therefore, might eventually prove fatal.
Cessation of respiratory airflow (apnea) may be central or diaphragmatic (ie, no respiratory effort), obstructive (usually due to upper airway obstruction), or mixed. While short central apnea (<15 seconds) can be normal at all ages, prolonged apnea that disrupts physiologic function is never normal. Some pathological evidence and ample theoretical evidence support central apnea as a cause for SIDS and an associated, if not key, role for obstructive apnea in some infants. Expiratory apnea (lung collapse) also has been proposed as a cause of SIDS; however, necropathologic evidence of its presence is found in only a small minority of cases.
Obstructive apnea
Developing infants have normal sites of anatomic and physiologic vulnerability that, alone or combined, may transiently dispose an infant to airway obstruction. Among these vulnerabilities are the shallow hypopharynx, the cephalad position of the tongue and epiglottis, and the more compliant rib cage.
Positioning may predispose the newborn to upper airway obstruction as well. While infants with anatomic anomalies are particularly at risk, obstruction may occur in those with normal anatomy. Most infants are obligate nasal breathers for the first few months of life. The nares flare anteriorly, with the nose forming no protrusion. Hypoxemia of sufficient severity to produce ECG evidence of cerebral hypoxia does not begin until 60-70 seconds after the onset of obstruction. Although infants placed in the prone position on a level sleeping surface may turn their faces to maintain oxygen flow, respiratory obstruction with compression of the nose and backward displacement of the mobile mandible has been implicated as a cause of asphyxia while in the prone position.
Gastroesophageal reflux (GER) may play a role in obstructive apnea as well. Regurgitation increases mucosal adhesive forces, a condition of significance in infants with their more pliable airways. Occurrence of this phenomenon in infants who have laryngeal inflammation secondary to chronic regurgitation increases their risk of obstructive apnea.

[Dr.Nathalie]

Central apnea
Unlike older children and adults, normal neonates and infants may suffer a reflexlike apneic response to a number of physiologic and pathophysiologic conditions such as hypoxia, hypoglycemia, intracranial bleeding, infection, some toxins, and stimulation of the upper larynx. GER's acid reflux may affect a putative laryngo-chemoreceptor, causing respiratory pause, airway closure, and swallowing. This may result in an awake apneic event, which is not uncommonly reported by parents.
Such apneic responses are probably due to incomplete development of the CNS, increased vagal tone, and decreased respiratory muscle reserve. While there is no statistical association between such episodes of apnea and SIDS, the potential for the immature nervous system to easily interrupt its respiratory cycle may be a critical precondition for SIDS shared by all normal infants.
Infants with subclinical dysfunction of the autonomic nervous system or those undergoing physiologic stress may be predisposed to fatal evolution of an otherwise benign episode of apnea. Hypoxia, hypercarbia, and other noxious stimuli normally cause arousal and generalized alertness of the musculoskeletal and nervous systems, in addition to tachypnea and gasping. This is followed by cycles of apnea alternating with a gasp. SIDS is rare during the first month of life, perhaps in part because neonates have a better aerobic capacity than older infants and a gasp may raise their PaO2 to over 20 mm Hg and allow them to continue breathing. If such is not the case, each gasp becomes weaker than the preceding one until terminal apnea and death occur. Indirect evidence supports the hypothesis that slowly progressive hypoxia inhibits protective ventilatory reflexes in normal infants. When these infants are acutely rechallenged, the result is hypoventilation and apnea, rather than a tachypneic response.
Acquired ventilatory dysfunction could explain the chronic tissue hypoxia seen in many infants who die from SIDS. Several, but not all, studies suggest that at-risk infants have subclinical impairment in ventilation that is midway between normal infants and those with central hypoventilation syndrome. Infants who demonstrate diminished ventilatory response to hypoxia and hypercapnia have significantly diminished arousal response. Such diminished arousal responses are correlated with future episodes of apnea that require resuscitation.
Death may result during abnormal sleep, from dysfunction of the brainstem, or during normal sleep, when a pathophysiologic setting incites a lethal cascade of events. Diminished arousal response has been identified in newborns who subsequently suffer an ALTE as well as asymptomatic siblings of infants who died from SIDS, suggesting that some cases are congenital. Such diminished arousal also may be seen in some healthy infants (who do not have impaired ventilation). Prone sleeping results in hypoxemia and hypercarbia, findings that attach special significance to these abnormal responses to subclinical hypoxemia and hypercarbia and their possible relationship to SIDS.
Infants at risk have a relative inability to awaken and remain awake from all stages of sleep. Term infants have more episodes of nonperiodic apnea during REM sleep, which is autonomically active, than during quiet sleep. Relaxation of respiratory and accessory muscles has been documented in conjunction with skeletal muscle relaxation during REM sleep. Infants who subsequently died of SIDS had significantly more REM-associated obstructive breathing events; however, sleep-related airway obstruction did not occur in high-risk infants as long as there was arousal. Increased respiratory effort, occasionally with transient obstructive apnea, has been noted during quiet, non-REM sleep. Other hypotheses
Behavioral theory
Developmental disability of infantile neurorespiratory control is posited, occurring during the transition period when protective subcortical reflexes are no longer present, and voluntary defensive responses mediated via the cortex (ie, those that allow reestablishment of ventilation when it has been compromised) have not yet been sufficiently learned. The thesis proposes that infants so affected manifest global passivity from ill-defined constitutional, arousal, or behavioral disabilities. Those infants, in turn, have less opportunity to respond, learn, and benefit from experience, including early exposure to normal (partial or brief) airway obstructions.
Primary autonomic nervous system instability
This theory proposes that apnea and bradycardia are the result of primary autonomic dysfunction or sympathetic imbalance.
Vertebral artery compression theory
Anatomical dissections have demonstrated that the vertebral arteries of infants are vulnerable to compression on neck extension or rotation. The structural factors productive of such compression are (1) the lateral mass on the superior surface of C1 is small and does not provide a good means of preventing downward compression of the vertebral arteries; (2) the arch of the atlas is smaller than the foramen magnum and may invert up into the foramen magnum during neck extension, with resultant compression of the vertebral arteries; (3) the ligamentous support for the atlantooccipital junction is poorly formed, with greater mobility in infants than in adults; (4) the vertebral artery lies exposed on the surface of C1 and not in a bony groove as in adults; and (5) the posterior atlantooccipital membrane is often thick and compresses the vertebral artery during extension because of its position immediately above the vertebral artery.
In approximately 40% of infants, flow in one vertebral artery is less than half that in the contralateral vessel; thus, if the larger vessel is occluded, the brainstem is jeopardized much more than if flow were bilaterally equal. If both vertebral arteries are compressed, flow continues, given normal anatomy, via the posterior communicating arteries of the internal carotids. However, flow through the posterior communicating arteries in infants is only 13% of basilar artery flow, and the brainstem is thereby placed at risk.
Immunopathogenesis theory
The peak incidence of SIDS occurs during the second to fourth months of life. Around the third month, a decrease is seen in the passive immunity conferred by the mother, as the infant's immune system is activated. Early active immunity triggers localized immunologic responses to several substances, including respiratory irritants and infectious agents, with the potential for bronchospasm, pulmonary edema, and cytokine-mediated effects such as fever. Raised concentrations of immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) have been recovered from infants who have died of SIDS but not from infants who have died from explained causes.
Infections and SIDS
The peak incidence of SIDS coincides with critical periods in the development of the immune system; at such a time, the infant might be transiently vulnerable to lethal infection. SIDS incidence increases in the winter, during viral epidemics in a community, and 2 weeks after viral infection. Compared with healthy control infants and infants who died of known causes, many infants who died of SIDS have toxigenic bacteria, such as Escherichia coli, Staphylococcus aureus, and Clostridium difficile, as well as influenza and respiratory syncytial virus (RSV). Most strongly implicated is RSV, which is well known for its association with central apnea.

[Dr.Nathalie]

Unstable homeostatic control
SIDS has been proposed to be the result of a developmental malfunction of brain stem centers that control respiratory and/or cardiac functions during sleep. This occurs as the body's thermostats change from fetal to mature mode, usually during the second to third months of life.
At some point in healthy infants aged 8-16 weeks, 2 sleep-related temperature patterns emerge: a precipitous drop in rectal temperature amounting to several tenths of a degree Celsius, followed by hourly oscillations throughout sleep. These temperature fluctuations are thought to herald maturation of the brainstem during the second to fourth months of life. The second through fourth months are also the peak time for occurrence of SIDS. Temperature maturation occurs earlier (closer to 8 wk than 16 wk) in infants who are breastfed and firstborn, who sleep in a lateral or supine position, whose mothers are older, and who are born into more affluent families (all factors associated with decreased incidence of SIDS). Oyen et al posit that preterm babies probably have a delay in their vulnerable period, because they die later than do term infants (mean ages of 19.6 wk and 15 wk, respectively).
As the baby grows, its heightened metabolism and increasing body fat prompt a shift from the neonate's susceptibility to cold stress toward increased vulnerability to heat stress in infancy. This occurs at about the same time as the highest risk for SIDS. This hyperthermic response may be aggravated by the increased metabolism seen during the early stages of a viral infection, as well as via interleukin-mediated vasoconstriction. The available evidence suggests that even small elevations in body temperature can have profound effects upon the respiratory rate, resulting in hypoventilation and apnea.

[Dr.Nathalie]

Triggering factors
Vulnerable periods in maturation of the brain stem may be critical when associated with the prone sleeping position. When sleeping prone, infants frequently assume a facedown position, especially in response to cold stimulus to the face. Healthy infants, aged to 6 months, were studied as they slept in the prone position on soft and firm bedding. Despite the fact that all infants were able to turn their heads from this position, they slept face down an average of 14% of total sleep time on hard bedding and 35% on soft bedding. The PaCO2 rose in all infants from rebreathing while face down, with inspired carbon dioxide higher in those on soft bedding.
Babies aged 13-24 weeks (the time of peak risk for SIDS) are more mobile than are younger infants; however, Oyen et al opined that they may not have the motor ability to extricate themselves from dangerous positions such as facedown on soft bedding. In another study of infants aged 3-37 weeks who never slept on their stomach, it was found that they do not learn the behaviors that may reduce their risk of SIDS if they are prone. In this study, researchers placed a comforter over a foam rubber mattress directly under the babies' faces. All babies awoke after approximately 5 minutes and sought fresher air. The babies with prone sleeping experience lifted and turned their heads to the side; however, the babies inexperienced in sleeping prone only nuzzled the bedding or briefly lifted their heads and then resumed sleeping facedown.
An infant sleeping prone, surrounded by a soft mattress, blankets, or other bedding, and possibly co-bedding with adults and compressed by or between large bodies, is in an environment that predisposes to progressive increase in carbon dioxide-rich, oxygen-poor air. The normal response to rebreathing expired air is increased ventilation and arousal, but with these normal responses blunted, hypoxia and hypercarbia may proceed unchecked.
A 1968 study, using the cadavers of infants aged 6-9 weeks who were found dead in their cribs, measured resistance to airflow pumped through the upper respiratory tract. When the body was placed face down on a pillow on various types of bedding, respiratory resistance increased by a 30- to 40-fold factor. Moisture of respiration, regurgitated milk, and mucus from the nostrils may dampen bedding material, with increased obstructive effect when that wet material is compressed against the mouth and nose. In fact, when the pillow was damp the mean increase in pressure was 235%.
Thermal stress and rebreathing carbon dioxide may share an interrelationship as contributors to SIDS. Hyperpnea secondary to rebreathing increases the production of heat; rebreathing warmed, expired air reduces respiratory heat exchange and enhances thermal stress; heat stress is presumably associated with an increased production of carbon dioxide, which could increase the risk of suffocation.
Sleeping in a hyperthermic environment also may alter the response to hypoxia or hypercarbia. An inadequate response to a critical incident may precipitate SIDS in a vulnerable infant who has acquired deficits in arousal or other physiologic aberrations in utero that are enhanced during postnatal development.
The dangers of prone sleeping also may stem from more episodes of quiet sleep, sleep for longer periods with fewer arousals, and decreased ability to lose heat, which is a phenomenon that may be enhanced by a heated room, excessive wrapping, fever, or illness.
Given the interrelationship between the risk of SIDS and increased temperature, why does the incidence of SIDS increase in cold temperature? Evidence suggests that autonomic dysfunction in at-risk infants is greatest at the lowest ambient temperature, even though body temperature remained normal. This cold-induced autonomic dysfunction may explain the association between SIDS and the cold ambient temperatures of winter.
An interesting correlation between several of the factors discussed above and the possibility of vertebral artery compression has been advanced.
With regard to the prone sleeping position, infants having the ability to do so will attempt to clear their nose from bedding by extending or rotating their head, the exact neck positions potentially productive of vertebral artery compression with resultant brainstem ischemia.
During the first months of life, the infant brainstem is particularly vulnerable to ischemia as a result of bloodflow lagging behind the rapidly growing brainstem. SIDS is not common before age 1 month or after age 6 months. Before the second month, infants may lack both the strength and coordination to rotate or extend their heads to the degree required for compression of the vertebral artery. By age 6 months, the adverse anatomy that may predispose to arterial compression has begun to resolve.
The vertebral arteries arise from the subclavian arteries; thus, the vertebrobasilar circulation is in competition with the vascular beds of the upper extremities for flow. Heating of the limbs has the potential to increase blood flow to the upper extremities by 4-5 times the norm, thus potentially diverting blood flow that would otherwise go to the vertebral arteries and necessitating vasodilation of the vertebrobasilar system to maintain constant flow to the posterior fossa.
Smoking is a risk factor for SIDS. Passive smoking has been found to impair vasodilatation in young adults. Should a similar mechanism be operative in infants, the vertebral arteries may lack the ability to dilate adequately to prevent subclavian steal resulting from overheating, as discussed above.
Synthesis
Most cases of SIDS probably result from a lethal sequence of events initiated by a temporary defect in neural control of either respiratory or cardiac function during vulnerable periods in the maturation of respiratory control, sleep-wake development, and thermoregulation. Cardiorespiratory function, arousal and gasp reflexes, autonomic mechanisms, chemoreceptor sensitivity, thermoregulation, and sleep control are all controlled by the medullary and related structures of the brainstem. Autopsy examinations of the brainstems of infants with a diagnosis of SIDS have demonstrated hypoplasia or decreased neurotransmitter binding of the arcuate nucleus, the region of the brain believed involved with hypercapnic ventilatory response, chemosensitivity, and blood pressure responses.
While the exact nature of possible brainstem dysfunction is unknown, hypotheses include exaggeration of the postulated developmental lag between loss of infantile protective neuroreflexes and the development of mature integrative connections in the brainstem. Alternatively, it has been proposed that brainstem dysfunction may be congenital, or they may be the result of arrested maturation of the otherwise normal brain by an internal or external agent. If this hypothesis is true, SIDS is an acquired and, therefore, potentially preventable cause of death.
Yet another hypothesis is that SIDS is the result of a transient, physiologically vulnerable period during maturation of a normal CNS in which the coincidence of several risk factors may cause apnea and death.
Irrespective of the exact mechanism, the infant responds to a range of stimuli, insults, and risk factors with prolonged apnea, bradycardia, and death. Such a theory sets the stage for a spectrum of brainstem pathologies that include the following:

• Infants with normally functioning brainstems at no risk for SIDS, no matter the nature or quantity of risk factors
• Infants with relatively minor brainstem dysfunction who will develop prolonged apnea and die only in the presence of multiple risk factors
• Infants with greater brainstem dysfunction who require only 1 additional risk factor (eg, additional warmth and decreased air circulation resulting from an extra blanket, benign viral infection that causes a relatively minor subglottic airway obstruction)
• Infants at the far end of the continuum whose brainstems are so dysfunctional that they will have virtually unprovoked SIDS
• This theory can incorporate other proposed SIDS mechanisms, such as abnormal infantile respiratory patterns leading to apnea, exaggerated vagal response to GER, sleep disorders, and autonomic dysfunction. This theory also can account for the variable epidemiologic and pathophysiologic findings and the frequent lack of demonstrable pathology at autopsy.

[Dr.Nathalie]

• 
  Frequency:
• In the US: SIDS is the most common cause of death in infants aged 1 month to 1 year, although incidence has shown a progressive decline since 1992. In that year, the incidence of SIDS was 1.2 cases per 1000 live births; in 2002, the incidence had dropped to 0.57. While cases of true SIDS are decreasing, concern exists that the proportion of unexplained infant deaths resulting from child abuse may be increasing. Notably, the American Academy of Pediatrics estimates that the incidence of infanticide among cases designated as SIDS ranges from less than 1-5%. In 2002, 2,295 deaths were certified as SIDS, accounting for 8% of infant deaths.
• Internationally: The incidence per 1000 live births in many Asian countries is 0.04. (Hong Kong has a rate of approximately 0.2.) Some Scandinavian countries have rates in the range of 0.2-0.6, and, in Italy, the incidence is 0.7. Prior to recommendation of the supine sleeping position, the United Kingdom had an incidence of 3.5 cases per 1000 live births (now reduced to 1.7), and New Zealand had an incidence of approximately 4.5.

Race:

• Risk among racial groups varies substantially. In 2002, SIDS rates were highest for American-Indian and non-Hispanic Black mothers, 2.2 and 2.0 times more respectively, than the rate for non-Hispanic White mothers. Contrasted with that was the SIDS rate for Mexican mothers, which was 48% lower, and Central and South American mothers who had a SIDS rate 62% lower, than the rate for non-Hispanic White mothers. Further data as to rates by race are as follows:
  • Central and South Americans - 0.21 cases per 1000 live births
  • Asian/Pacific Islanders - 0.24 cases
  • Mexicans - 0.29 cases
  • Puerto Ricans - 0.54 cases
  • Whites - 0.55 cases
  • African Americans - 1.11 cases
  • American Indian - 1.23 cases

Sex: Approximately 60-70% of SIDS deaths occur in males.
Age:

• Approximately 80% of deaths occur in infants younger than 5 months, with a peak incidence in infants aged 2-4 months. Only 1% of deaths occur in neonates. The remainder of deaths are noted after the sixth month of life.

• Prior to adoption of the current case definition, 3% of SIDS deaths were reported after the first year of life.

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Ну и так далее.

[Andru]

Наталья Рашидовна большое спасибо, переведу месяца через 3-4, да где то так (очень плохо с аглицким языком).

[vlg_asb]

Сдавление позвоночной артерии в результате изменения положения головы - возможная причина синдрома внезапной смерти.

Pediatrics. 1999; 103(2):460-8 (ISSN: 1098-4275) [Ссылки доступны только зарегистрированным пользователям ]

Pamphlett R ; Raisanen J ; Kum-Jew S
Neuropathology Unit, Department of Pathology, University of Sydney, Sydney.

ЦЕЛЬ:Высказывались предположения, что в основе синдрома внезапной детской смерти лежит стволовая ишемия, происходящая в бассейне позвоночных артерий. Во время ангиографии у детей было продемонстрировано, что при движении головы имеет место изгиб позвоночных артерий, но прямых доказательств того, что артерии сдавливаются при этом ─ не было. Для того чтобы продемонстрировать компрессию позвоночных артерий при изменении положения головы, было изучено посмертное состояние вертебральных артерий в патологоанатомических препаратах детей, голова которых была запрокинута или повернута.
МЕТОДЫ: У 20 детей, умерших от внезапной детской смерти или других причин, были выделены препараты на уровне C1-C7 позвонков, включая 2х-сантиметровый ободок в основании черепа. В 5 случаях голова была запрокинута, в 9 случаях ─ повернута на 90 градусов вправо, и в 6 случаях ─ находилась в нейтральной позиции. Препараты были зафиксированы в этом положении формалином, и просмотрены под микроскопом послойно.
РЕЗУЛЬТАТЫ: В 3 из 5 случаев экстензии отмечалось двухстороннее ущемление позвоночных артерий между затылочной костью и С1 позвонком. В 3х из 9 случаев ротации, левая позвоночная артерия оказалась сдавленной на уровне C1 в месте вхождения в foramen transverse. Не было отмечено сдавления позвоночной артерии, когда голова находилась в нейтральной позиции. ВЫВОДЫ: У некоторых младенцев позвоночные артерии могут быть пережаты при изменении положения головы. Это может вызвать смертельно опасную ишемию ствола мозга у детей с недостаточно развитой сетью коллатеральных сосудов или с нарушенным компенсаторным механизмом артериальной дилатации, что может лежать в основе некоторых случаев синдрома внезапной детской смерти.

[dr.Ira]

Сообщение от vlg_asb

МЕТОДЫ: У 20 детей, умерших от внезапной детской смерти или других причин,

Во-первых, этой статье уже 20 лет.

Во-вторых, SIDS потому и представляет проблему, что там нет

Сообщение от vlg_asb

или других причин

У меня нет доступа к оригиналу, но, либо некорректна статья, либо Вы некорректно перевели.
На postmortum у этих детей не обнаруживается никакой патологии. Потому что, если патология обнаруживается, то это уже не SIDS.
Наверняка, есть какой-то триггер, запускающий механизм SIDS, но, как известно, когда теорий много, этиологическая причина неясна.
На сегодняшний день известно только несколько факторов, позволяющих предположить их участие в развитии SIDS и позволяющих предположить, что, если придерживаться определенных правил, то, возможно, можно снизить риск SIDS, но нельзя исключить.

[vlg_asb]

The C1-C7 spinal column, together with a 2-cm rim of skull base, was removed from 20 infants dying from sudden infant death syndrome or other causes
See: [Ссылки доступны только зарегистрированным пользователям ]

[dr.Ira]

Вы перевели правильно. Некорректна статья. Не все, что печатается на англ., справедливо.

[vlg_asb]

SIDS - Неожиданная, необъяснимая смерть младенца во сне.
Т.о. любой, кто найдет причину этого явления – ставит под сомнение диагноз SIDS, точнее, отвергает его.
Абсурдны даже попытки найти единую причину SIDS с точки зрения лингвистики.
Шаманизм инициаторов “Back to sleep», которые бросили призыв: «не кладите ребенка спать на живот!» состоит в том, что они не понимают, почему так сказали, но это удивительным образом привело к сокращению случаев неожиданной смерти детей во сне.
Мы не знаем и никогда не узнаем, почему здоровые дети неожиданно умирают во сне, да это и не нужно. Главное, знать, что этому предрасполагает. Многофакторные эпидеимологические исследования, изучающие окружение ребенка от положения его во сне и курит ли его мама до факта, какой преобладающий день недели, когда это происходит(знаете ли вы, что это выходные дни?) – корректнее конкретных патологоанатомических исследований.
Попробуем с точки зрения переводчика исправить некорректность, допущенную авторами исследования, которому 20 лет, хотя оно выполнено в 1999 году: Для исследования были выбраны 20 неожиданно умерших детей, как тех, которые до этого внешне были здоровы, так и тех у которых предполагаемая причина для смерти была.
Кажется, это не скажает смысла оригинала, но звучит более корректно?

[riltsov]

У меня нет доступа к оригиналу

[Ссылки доступны только зарегистрированным пользователям ] обсуждаемой статьи.