ATP-Depletion durch Hyperventilation, Gewebehypoxie und Hypermetabolismus als Ursache für Plötzlichen Kindstod – eine Hypothese

Zusammenfassung

Einleitung: Trotz rückläufiger Inzidenz ist der Plötzliche Kindstod in den Industrienationen noch immer die häufigste Todesursache im ersten Lebensjahr. Pathogenetisch spielt Hypoxie eine wichtige Rolle, der genaue Mechanismus ist allerdings ungeklärt.

Methoden: Eigene Überlegungen und selektive Literaturrecherche im Internet.

Hypothese: Der Plötzliche Kindstod ist Folge einer häufig protrahiert verlaufenden ATP-Depletion.

Diskussion: Sämtliche Risikofaktoren für Plötzlichen Kindstod begünstigen, besonders in Kombination, einen ATP-Mangel, indem sie den ATP-Abbau beschleunigen und/oder die ATP-Synthese vermindern. Pränataler chronischer Sauerstoff- und Nährstoffmangel führt beim Neugeborenen zu niedrigerem Geburtsgewicht, vermindertem Fettgewebe, vermehrtem Hämoglobin F, erhöhtem Sympathikotonus, Hypermetabolismus und reduzierter Hypoxietoleranz. Aufgrund geringerer Fettreserven wird postnatal mehr Energie für Wärmebildung benötigt, und bei Sauerstoffmangel zeigen Risikokinder einen abgeschwächten hypoxischen Hypometabolismus mit Hyperventilation statt Atemdepression. Die dadurch vermehrte Atemarbeit erfordert zusätzliche Energie und führt über eine weitere Zunahme der in diesem Lebensalter physiologischerweise noch erhöhten Sauerstoffaffinität zu Gewebehypoxie und verminderter ATP-Synthese. Zusätzlich verursacht der erhöhte Sympathikotonus Hypermetabolismus und beschleunigten ATP-Abbau. Während angeborene Risikofaktoren in Belastungssituationen, wie Nahrungsmangel, zu einer reduzierten ATP-Produktion führen können, erhöhen postnatale Risikofaktoren, wie zum Beispiel Überwärmung und Stress, durch Hyperventilation und Stoffwechselsteigerung den ATP-Umsatz und entleeren die Energiespeicher. Der Häufigkeitsgipfel für das Auftreten des Plötzlichen Kindstodes bei reifen Neugeborenen lässt sich durch den Hämoglobintiefpunkt der physiologischen Anämie und die dadurch verminderte Sauerstofftransportkapazität des Blutes erklären, welche die Gefahr einer Gewebehypoxie als Folge der noch erhöhten Sauerstoffaffinität und der nachlassenden Fähigkeit zu hypoxischem Hypometabolismus weiter vergrößert. Nahezu identische Befunde von Plötzlichem Kindstod einerseits und ATP-Mangelerkrankungen, wie zum Beispiel Hypophosphatämie, Hitzschlag und Kohlenmonoxidvergiftung andererseits, untermauern die aufgestellte Hypothese.

Abstract

Introduction: Despite a decreasing incidence, sudden infant death syndrome (SIDS) is still the most frequent cause of death in industrial nations during the first year of life. Hypoxia plays a major role in the pathogenesis, but the exact mechanism is not fully understood.

Methods: This study was based on personal considerations and a selective online literature search.

Hypothesis: SIDS is the result of a frequently protracted ATP-depletion.

Discussion: Especially in combination, all risk factors for SIDS favour an ATP-deficiency by increasing ATP-catabolism and/or by diminishing ATP-synthesis. Prenatal chronic hypoxaemia and an insufficient supply with nutrients lead to low birth-weight, reduced adipose tissue, elevated haemoglobin F, increased sympathetic activity, hypermetabolism, and diminished hypoxia tolerance in the neonates. Because of reduced adipose tissue, more energy for thermogenesis is needed after birth. In reaction to hypoxaemia, infants with risk factors show hyperventilation instead of hypoxic hypometabolism and respiratory depression. Enhanced breathing, however, requires additional ATP and causes increasing oxygen affinity, which is elevated physiologically during the first months of life. Thereby, tissue-hypoxia and diminished ATP-synthesis may arise. Besides, enhanced sympathetic activity leads to hypermetabolism and increased ATP-catabolism. While innate risk factors may reduce ATP-production in burdening situations, like food deprivation, postnatal hyperthermia and stress augment ATP-catabolism by hyperventilation and hypermetabolism and empty energy stores. For term newborns, the peak incidence of SIDS might be explained by the haemoglobin nadir of physiological anaemia and by the therefore reduced capacity for oxygen transport. Thereby, the risk of tissue-hypoxia, which follows increased oxygen affinity and vanishing ability to hypoxic hypometabolism, is further enhanced. The almost identical symptoms of SIDS and ATP-deficiency diseases like hypophosphataemia, heat stroke, and carbon monoxide poisoning support the presented hypothesis.

Schlüsselwörter

Plötzlicher Kindstod - Gewebehypoxie - Hypermetabolismus - ATP-Depletion

Key words

sudden infant death syndrome - tissue-hypoxia - hypermetabolism - ATP-deficiency

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