ABSTRACT
Over the 10-year period studied, a total of 96 children under 15 years of age were killed in Sweden. This number constituted an average annual rate of 0.6 per 100,000 children. The violence, most frequently involving strangulation, shooting, and stabbing, was largely directed at young children. The pattern of child homicide was mainly characterized by intrafamilial violence, especially in connection with the suicide of a parent-perpetrator. Extrafamilial homicides were rare and only committed by male perpetrators. Cases of child abuse by a parent and cases of sexual abuse were infrequent. By psychiatric examination after the crime, only 10 perpetrators out of 47 examined were found not mentally ill.
Subject(s)
Cause of Death , Child Abuse, Sexual/mortality , Child Abuse/mortality , Homicide/trends , Infanticide/trends , Adolescent , Child , Child Abuse/legislation & jurisprudence , Child Abuse/prevention & control , Child Abuse, Sexual/legislation & jurisprudence , Child Abuse, Sexual/prevention & control , Child, Preschool , Female , Homicide/legislation & jurisprudence , Humans , Infant , Infant, Newborn , Infanticide/legislation & jurisprudence , Infanticide/prevention & control , Male , Suicide/trends , Sweden/epidemiologyABSTRACT
Tissue thromboplastin probably plays an important role in the development of post-traumatic pulmonary microembolism. Infusion of purified human tissue thromboplastin in animals resulted in an intravascular coagulation and respiratory insufficiency. This could be inhibited by previous infusion of phospholipase C (PLC) from Bacillus cereus. We have studied the effects of PLC infusion on the course of post-traumatic pulmonary microembolism, induced by a high-energy (c. 700 J) missile trauma to the hind legs of pigs. The trauma resulted in a major muscular injury and an indirect femoral fracture. Untreated pigs developed intrapulmonary microemboli. The degree of microembolism in the lungs was measured quantitatively by external detection over the right lung of radiolabeled platelets and fibrin. Infusion of 80 micrograms PLC/kg/hour resulted in an accumulation of blood PLC associated with toxic reaction leading to increasing tachycardia and circulatory collapse after 10 hours. PLC infusion of 20 micrograms/kg/hour did not inhibit the pulmonary microembolism. A PLC-dose in between, viz. 40-50 micrograms/kg/hour, proved to efficiently inhibit most of the microembolism during the infusion period. Cessation of PLC infusion after 24 hours was accompanied by a later increase in pulmonary trapping of platelets and fibrin and decreases in paO2. Concomitantly there were opacities seen on chest X-rays. The results show that tissue thromboplastin is an important etiologic factor in post-traumatic pulmonary microembolism and that inhibition with phospholipase C can be of value in the prophylaxis of the syndrome.
