This page describes the treatment method for hypoxic encephalopathy on the homepage of the Japanese Society of Emergency Medicine.

Here you will find the following:

Postresuscitation encephalopathy patients with cardiac arrestoften develop invasive hyperglycemia and hyperthermia due to hypermetabolism, and these hyperglycemia and hyperthermia are important factors that worsen the neurological outcome. Therefore, it is necessary to prevent and manage these, and to minimize secondary brain damage by appropriate respiratory and circulatory management. In recent years, it has been reported that in patients with cardiac arrest who continue to be in a coma after resuming their own heartbeat, the functional outcome may be improved by performing brain hypothermia.

That is, hyperglycemia and hyperthermia, which are important factors that worsen the neurological outcome, occur in patients with encephalopathy. These hyperglycemia and hyperthermia are promptly managed and appropriate respiratory and circulatory management (appropriate respiratory and circulatory management) It is necessary to minimize secondary encephalopathy with a ventilator). Is written.

However, Jimmy did not use any cooling (such as ice pillows) to lower the temperature of 42 degrees, no fever-lowering medications, and no treatments or medications to lower more than 300 hyperglycemias. If you have a high fever of 42 degrees and high blood sugar for 20 hours, even a healthy brain will be damaged. Sometimes you die. But they left it untreated.

Indeed, it is an unnecessarily intentional and abandonment of the person responsible for protection in an attempted murder.

I don't know why the police aren't investigating.

The following is an excerpt from the website of the Japanese Society of Emergency Medicine.

Treatment required for hypoxic encephalopathy

Hypoxic encephalopathy is a condition in which the brain is damaged due to insufficient oxygen supply due to circulatory failure or respiratory failure. Hypoxemia is usually a mixture of two conditions: decreased blood flow to tissues (ischemia) and decreased blood oxygen carrying capacity (hypoxemia). It is also called hypoxic-ischemic encephalopathy. Causes include myocardial infarction, cardiac arrest, various shocks, and suffocation . When the oxygen supply to the brain is interrupted due to cardiac arrest, consciousness disappears within a few seconds, and in cardiac arrest of 3-5 minutes or longer, even if self-heartbeat resumes, brain damage (postresuscitation encephalopathy) occurs. Factors predicting poor outcome of postresuscitation encephalopathy include the appearance of myoclonus and status epilepticus within 24 hours after resumption of self-heartbeat, loss of pupillary response and corneal reflex, and loss of motor response or limb abnormalities 3 days later. There is an extension reaction.

As a treatment, simply maintaining blood pressure does not lead to improvement in survival rate and rehabilitation rate , and it is important to maintain blood flow to organs and peripheral tissues throughout the body. Furthermore , postresuscitation encephalopathy patients with cardiac arrest often develop invasive hyperglycemia and hyperthermia due to hypermetabolism, and these hyperglycemia and hyperthermia are important factors that worsen the neurological outcome. Therefore, it is necessary to prevent and manage these, and to minimize secondary brain damage by appropriate respiratory and circulatory management. In recent years, it has been reported that in patients with cardiac arrest who continue to be in a coma after resuming their own heartbeat, the functional outcome may be improved by performing brain hypothermia.