Child fatalities

Chance, T. and Scannapieco, M. (2002) Ecological correlates of child maltreatment similiarities and differences between child fatality and non-fatality cases. Child and Adolescent Social WorkJournal 19, 139-161. 

Dietary Copper. Analytical data indicate that many diets contain less than the RDA for copper (109). Excessive copper has been reported to be fatal for oral dose levels of copper sulfate of 200 mg/kg body weight for a child and 50 mg/kg for adults. 

Although extraordinary in its powers, aspirin is also more dangerous than commonly believed. Only about 15 g can be fatal to a small child, and aspirin can cause stomach bleeding and allergic reactions in long-term users. Even more serious is a condition called Reye s syndrome, a potentially fatal reaction to aspirin sometimes seen in children recovering from the flu. As a result of these problems, numerous other NSAIDs have been developed in the last several decades, most notably ibuprofen and naproxen. 

Of greater concern is the safety of the TCAs. Toxic levels of these medications can produce lethal cardiac arrhythmias, seizures, and suppression of breathing. An overdose of a 1-2 week supply of most TCAs is often fatal, a serious consideration when prescribing medication to depressed patients with suicidal thoughts. Children taking imipramine for treatment of ADHD have died from sudden cardiac death consequently, child psychiatrists seldom use TCAs. Likewise, patients with heart disease or seizure disorders are more likely to have dangerous complications from TCAs and should avoid them. 

Other approaches to induce gastrointestinal discomfort have far more serious toxic effects. The chemical colchicine stops cell division (an antimitotic), producing severe nausea, vomiting, and dehydration, which can lead to delirium, neuropathy, and kidney failure. On the other hand, colchicine is used in the treatment of gout and has been studied as an anticancer agent because it stops cell division. Most toxic of all are plants that produce lectins, and the most toxic of these is the chemical ricin produced by castor beans. Only 5 to 6 seeds are necessary to kill a small child. Fortunately, following oral consumption much of the ricin is destroyed in the stomach. Ricin is extremely effective at stopping protein synthesis, so much so that direct exposure to only 0.1 pg/kg can be fatal. 

Parathion is the materiai of this type most frequently involved in fatal human poisonings. 0.1 mg/kg can kill a 5-6 year old child. 

Kwashiorkor usually occurs in the second or third year in the life of a child. Edema is the principal symptom. The condition arises from a combination of circumstances, but the primary cause appears to be a weaning diet that is both inadequate and indigestible and, notably, is lacking of protein. The principal calories are supplied by carbohydrate. The condition is accelerated by repeated infections of a bacterial, parasitic, or vital nature. Without treatment, the disease is fatal in most cases. 

Fatal gastroschisis occurred in a child bom to a mother who had taken high-dose carbimazole (60 mg/day) during the first trimester of pregnancy (97). 

Propofol infusion syndrome might be precipitated by a combination of prolonged propofol infusion and carbohydrate intake insufficient to suppress fat metabolism. Support for this hypothesis has come from a case report of a child with catastrophic epilepsy who developed fatal propofol infusion syndrome after a ketogenic diet was introduced in an attempt to control severe intractable epilepsy (962). 

This toxic protein is contained in caster seeds but does not pass into the oil. Similar phytotoxins occur in croton seeds (Crotin) jequirity seeds (Abrin) the bark of the locust tree, Robinia pseudo-acacia (Robin) and in the seeds of some leguminous plants (Phasin). The last is but weakly toxic. Ricin is responsible for the toxic effects on eating castor seeds 5 or 6 of these are fatal to a child, 20 to adults, and 3 or 4 seeds may cause violent gastroenteritis with nausea, headache, persistent vomiting, colic, sometimes bloody diarrhea, thirst, emaciation, and great debility. The symptoms usually do not set in until after several days. More severe intoxications cause small frequent pulse, cold sweat, icterus, and convulsions. Death occurs in 6 to 8 d, from the convulsions or from exhaustion. The fatality rate is about 6%. This low fatality rate is due to the destruction of the poison in the alimentary canal. The treatment would be evacuant and symptomatic. Usually, 3 to 10 d are required to complete recovery. 

T2. Thatcher, L., Hypervitaminosis D with report of fatal case in child. Edinburgh Med. J. 38, 457-467 (1931). 

Macdougall, C. F., Cant, A. J., and Colver, A. F. 2002. How dangerous is food allergy in childhood The incidence of severe and fatal allergic reactions across the UK and Ireland. Arch Dis Child 86 236-239. 

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