Sudden infant death

Biotin 0.15-0.3 mg/day. The discovery that biotin deficiency in young chickens can lead to sudden death resulted in a recommendation to supplement infant formulations with biotin.3 Desthiobiotin, in which the sulfur has been removed and replaced by two hydrogen atoms, can replace biotin in some organisms and appears to lie on one pathway of biosynthesis. b/C Oxybiotin, in which the sulfur has been replaced by oxygen, is active for many organisms and partially active for others. No evidence for conversion to biotin itself has been reported, and oxybiotin may function satisfactorily in at least some enzymes. 

As an example, my wife, who is a nurse specializing in neonatology, once told me about a premature infant who had died on her shift. The death had saddened her deeply. I felt a little sadness, said a sympathetic word, and put the matter out of my mind. A minute later I noticed that I had suddenly developed a headache. The news of the infant s death had actually touched me deeply, had been fully received and evaluated by my emotional brain, but my intellectual brain, preoccupied with its plans for the day, had handled the news intellectually instead of allowing my emotional brain to work properly. The resulting interference by the head with the appropriate heartache resulted in a headache. 

The safety of oral propafenone in the treatment of dysrhythmias has been studied retrospectively in infants and children (40). There were significant electrophysiolo-gical adverse effects and prodysrhythmia in 15 of 772 patients (1.9%). These included sinus node dysfunction in four, complete atrioventricular block in two, aggravation of supraventricular tachycardia in two, acceleration of ventricular rate during atrial flutter in one, ventricular prodysrhythmia in five, and unexplained sjmcope in one. Cardiac arrest or sudden death occurred in five patients (0.6%) two had a supraventricular tachycardia due to Wolff-Parkinson-White syndrome the other three had structural heart disease. Adverse cardiac events were more common in the presence of structural heart disease and there was no difference between patients with supraventricular and ventricular dysrhythmias. 

Money DFL. 1970. Vitamin E and selenium deficiencies and their possible etiological role in the sudden death in infants syndrome. N Z Med J 71 32-34. 

Secondhand tobacco smoke has long been associated with respiratory disease in children. The WHO has estabhshed that secondhand smoke can cause sudden death in infants [27] and it has been recently reported that children exposed to it may be at greater risk for developing atherosclerosis as adults [28],... 

Denborough, M.A., Galloway, G.J., Hopkinson, K.C. (1982). Malignant hyperpyrexia and sudden infant death. Lancet 2, 1068-1069. 

True. Nicotine, carbon monoxide and other harmful chemicals from the burning tobacco travel in the mother s bloodstream and can reach the foetus. This can result in impaired development and reduced birth weight. Tobacco smoke can also be harmful to young children and babies (sudden infant death syndrome). 

SIDS Sudden infant death syndrome TMJ Temporomandibular joint... 

Drasch GA, Kretschmer E, Lochner C. 1988. Lead and sudden infant death Investigations on blood samples of SID babies. Eur J Pediatr 147 79-84. 

Haglund B, Cnattingius S. 1990. Cigarette smoking as a risk factor for sudden infant death syndrome A population-based study. Am J Public Health 80 29-32. 

SIDS (sudden infant death syndrome) Commonly known as cot death. 

The diphtheria, pertussis, and tetanus (DPT) vaccine, which has prevented more than 95% morbidity from these diseases, has been linked with convulsions, encephalitis, and sudden infant death syndrome. ... 

Jonville-Bera, A.P., Autret-Leca, E., Barbeillon, R, and Paris-Llado, J., Sudden unexpected death in infants under three months of age and vaccination status a case-control study, Br. J. Clin. Pharmacol, 51, 271-276, 2001. 

Aim B, Milerad J, Wennergren G, Skjaerven R, Oyen N, Norvenius G, Daitveit AK, Helweg-Larsen K, Markestad T, Irgens LM. (1998). A case-control study of smoking and sudden infant death syndrome in the Scandinavian countries, 1992 to 1995. The Nordic Epidemiological SIDS Study. Arch Dis Child. 78(4) 329-34. 

Ford RP, Schluter PJ, Mitchell EA, Taylor BJ, Scragg R, Stewart AW. (1998). Fleavy caffeine intake in pregnancy and sudden infant death syndrome. New Zealand Cot Death Study Group. Arch Dis Child. 78(1) 9-13. 

Schellscheidt J, Oyen N, Jorch G. (1997). Interactions between maternal smoking and other prenatal risk factors for sudden infant death syndrome (SIDS). Acta Paediatr. 86(8) 857-63. 

Failure to synthesise sufficient surfactant or the synthesis of abnormal surfactant, so that surface tension cannot be lowered, may play a role in several conditions respiratory distress syndrome of the newborn sudden infant death ( cot death ) and adult respiratory distress syndrome. The enzymes involved in the synthesis of surfactant only appear during the third trimester of pregnancy, so that surfactant is not produced in premature babies and they have difficulty breathing. 

Caffeine and theophylline are more active on the central nervous system, while theobromine is much less active. Caffeine and theophylline also appear to stimulate the respiratory centers, making them useful in the treatment of infants who stop breathing for extended periods of time (sleep apnea), which can lead to sudden infant death. 

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