When first presenting for treatment, the patient can be fully aware of their abuse as an event, but their appraisal of it is often distorted, such as believing that the event was unremarkable (a form of isolation). Frequently, victims do not make the connection between their abuse and their present pathology. Prevention
Child sexual abuse prevention programmes were developed in the United States of America during the 1970s. Some programme are delivered to children and can include one-to-one work and group work. Programmes delivered to parents were developed in the 1980s and took the form of one-off meetings, two to three hours long. In the last 15 years, web-based programmes have been developed. School-based education programs were evaluated in 2015 by Cochrane that demonstrated improvements in protective behaviors and knowledge among children. Offenders
Demographics
Offenders are more likely to be relatives or acquaintances of their victim than strangers. A 2006–07 Idaho study of 430 cases found that 82% of juvenile sex offenders were known to the victims (acquaintances 46% or relatives 36%).More offenders are male than female, though the percentage varies between studies. The percentage of incidents of sexual abuse by female perpetrators that come to the attention of the legal system is usually reported to be between 1% and 4%. Studies of sexual misconduct in US schools with female offenders have shown mixed results with rates between 4% to 43% of female offenders.
Physical injuries
Electric shock
Hyperpyrexia, and radiation

Mechanism
Most forms of myocarditis involve the infiltration of heart tissues by one or two types of pro-inflammatory blood cells, lymphocytes and macrophages plus two respective descendants of these cells, NK cells and macrophages. Eosinophilic myocarditis is a subtype of myocarditis in which cardiac tissue is infiltrated by another type of pro-inflammatory blood cell, the eosinophil. Eosinophilic myocarditis is further distinguished from non-eosinophilic myocarditis by having a different set of causes and recommended treatments. Coxsackie B, specifically B3 and B5, has been found to interact with coxsackievirus-adenovirus receptor (CAR) and decay-accelerating factor (DAF). However, other proteins have also been identified that allow Coxsackieviruses to bind to cardiac cells. The natural function of CAR and mechanism that the Coxsackievirus uses to infect the cardiac muscle is still unknown. The mechanism by which coxsackie B viruses (CBVs) trigger inflammation is believed to be through the recognition of CBV virions by Toll-like receptors.The binding of the SARS-CoV-2 virus through ACE2 receptors present in heart tissue may be responsible for direct viral injury leading to myocarditis. In a study done during the SARS outbreak,  SARS virus RNA  was ascertained in the autopsy of heart specimens in 35% of the patients who died due to SARS. It was also observed that an already diseased heart has increased expression of ACE2 receptor contrasted to healthy individuals. Hyperactive immune responses in COVID-19 Patients may lead to the initiation of the cytokine storm. This excess release of cytokines may lead to myocardial injury.