They state that non-pedophilic offenders tend to offend at times of stress; have a later onset of offending; and have fewer, often familial, victims, while pedophilic offenders often start offending at an early age; often have a larger number of victims who are frequently extrafamilial; are more inwardly driven to offend; and have values or beliefs that strongly support an offense lifestyle. One study found that pedophilic molesters had a median of 1.3 victims for those with girl victims and 4.4 for those with boy victims. Child molesters, pedophilic or not, employ a variety of methods to gain sexual access to children. Some groom their victims into compliance with attention and gifts, while others use threats, alcohol or drugs, or physical force. History
Pedophilia is believed to have occurred in humans throughout history, but was not formally named, defined or studied until the late 19th century. The term paedophilia erotica was coined in an 1886 article by the Viennese psychiatrist Richard von Krafft-Ebing but does not enter the authors Psychopathia Sexualis until the 10th German edition. A number of authors anticipated Krafft-Ebings diagnostic gesture. In Psychopathia Sexualis, the term appears in a section titled "Violation of Individuals Under the Age of Fourteen", which focuses on the forensic psychiatry aspect of child sexual offenders in general. Krafft-Ebing describes several typologies of offender, dividing them into psychopathological and non-psychopathological origins, and hypothesizes several apparent causal factors that may lead to the sexual abuse of children.Krafft-Ebing mentioned paedophilia erotica in a typology of "psycho-sexual perversion".
They also activate the coagulation cascade (blood clotting system) via factor XII, which can lead to disseminated intravascular coagulation and kidney damage. Isohemagglutinins also activate the complement cascade via C3a and C5a, which then promote inflammatory cytokine release from white blood cells. These inflammatory cytokines include IL-1, IL-6, IL-8, and TNF-alpha, which cause symptoms of low blood pressure, fever, chest pain, nausea, vomiting, and wheezing. Diagnosis
The diagnosis of AHTR is made with microscopic examination of the recipients blood and a direct antiglobulin test. The donor and recipient blood can be re-tested with a type, crossmatch, and antibody screen to determine the cause of the reaction. Treatment
Initial treatment for any type of transfusion reaction, including AHTR, is discontinuation of the transfusion. Fluid replacement and close monitoring of vital signs are important. People with AHTR are managed with supportive care, which may include diuretics, blood pressure support, and treatment of disseminated intravascular coagulation (with fresh frozen plasma, cryoprecipitate, and platelet transfusion). Furosemide is the diuretic of choice in treatment of AHTR with decreased urine output, because it increases the amount of blood that reaches the renal cortex. Mannitol may also be used. Dopamine is used for blood pressure support because it causes vasodilation (dilation of blood vessels) in the kidneys as well as increasing the cardiac output (amount of blood pumped by the heart each minute). Prognosis
The severity and prognosis of acute hemolytic transfusion depends on the rate of blood administration and the total volume of the transfusion. Approximately 2% of cases are fatal.