This page summarizes the in-hospital clinical course from 24 August 2010, when my father developed acute myocardial infarction and was transported to Toride Kyodo Hospital (now JA Toride General Medical Center) in Toride City, Ibaraki Prefecture, through percutaneous coronary intervention (PCI), shock, cardiac tamponade, hemothorax, and acute subdural hematoma, up until his death on 12 September 2010, as well as the results of analysis of charts and medical records obtained through a court-ordered evidence preservation procedure.
Overview of the In-Hospital Course and Analysis of Medical Records
Here we summarize the in-hospital course from 24 August 2010, when my father developed myocardial infarction and was transported to the hospital, through PCI (percutaneous coronary intervention), until his death on 12 September, along with analysis of charts and medical records obtained during the evidence preservation procedure.
The hospital in question is “Toride Kyodo Hospital” in Toride City, Ibaraki Prefecture. Six months after my father’s death, on 1 April 2011 (the fiscal year changeover), the hospital’s name was changed to “JA Toride General Medical Center”.
Clinical Course and Explanations from Physicians
- 2010
- 24 August: Onset of myocardial infarction and PCI
My father developed myocardial infarction and was transported by ambulance to “Toride Kyodo Hospital” (now JA Toride General Medical Center) in Toride City, Ibaraki Prefecture. PCI (percutaneous coronary intervention) was performed. The procedure took three hours to complete. The doctor explained, “The treatment was successful, but because the original myocardial infarction was severe, his subsequent course may be difficult.” My father was fully conscious and said, “I’m glad you brought me here. The doctor took time and did the procedure carefully,” expressing his relief. After the procedure, the attending doctor was chatting with other physicians. - 25 August: Low blood pressure and tachycardia, consciousness preserved
Despite multiple vasopressors being administered, his blood pressure remained low and he was tachycardic. My father was conscious. The doctor said, “His condition is quite severe.” I believed, “He will get better from here.” - 26 August: Deterioration, transfusion, and start of mechanical ventilation
We received an emergency call from the hospital. The doctor asked, “His condition has worsened. Do you wish to pursue aggressive treatment?” I answered, “Of course we do.” A blood transfusion was started because he was anemic (no explanation was given for the cause of the anemia). He was intubated and placed on mechanical ventilation. Because the time from symptom onset to PCI initiation had been short, I believed, “He will surely recover.” - 27 August: Severe shock and critical condition
We received another emergency call from the hospital. Around 3:00 p.m., his blood pressure was 60/40 mmHg and heart rate 150–160/min. The explanation was: “He is in extremely critical condition. Because the myocardial infarction was severe, the pumping function of his heart has decreased and blood pressure cannot be maintained. We are using vasopressors at the upper limit of the dose range. If we cannot maintain his blood pressure with these, there are no remaining treatment options. There is a high chance he will die today or tomorrow.” We visited again around 7:00 p.m. His condition was unchanged, and the doctor gave essentially the same explanation. On the doctor’s advice that “He will most likely pass away tonight, so please stay with him,” I replied, “That cannot be. I firmly believe he will recover. Please continue to provide the best possible treatment,” and we three family members left the hospital. - 28 August: Post hoc report of pericardiocentesis for cardiac tamponade
When we went to visit him in the morning, his blood pressure was 110/60 mmHg and heart rate 100/min. He had recovered from the state of shock. The attending physician reported after the fact, “Around midnight, he developed cardiac tamponade, so we performed pericardiocentesis.” The doctor explained, “The cause was oozing-type ventricular rupture—blood was slowly leaking into the pericardial sac through a gap in the infarcted, fragile myocardium—so his condition remains extremely dangerous.” When I asked, “Why did you not call us by phone to inform us of such a critical procedure?” the doctor replied, “We didn’t have the time to call,” which did not make logical sense. (This was the first time the term “cardiac tamponade” appeared. Until then, the doctor had never mentioned it. This led us to suspect that cardiac tamponade had been missed earlier. However, at that time we refrained from pursuing this, out of concern that my father might be treated less favourably if we confronted them.) - 5 September: Sedatives turned off
- 9 September: Weaned from mechanical ventilation, but consciousness did not return
He was extubated and taken off the ventilator. Regarding why consciousness did not return, the attending doctor explained, “Because his liver function is poor, the sedatives may be taking longer than usual to clear,” and “He may have had a stroke,” avoiding mention of the more likely main cause—hypoxic brain damage due to shock. - 11 September: Deterioration and questioning the doctor: “Was cardiac tamponade missed?”
As usual, we visited my father in the evening. He still had not regained consciousness. His face trembled and he appeared to be suffering. It was said that the attending doctor had gone home despite knowing this condition, so we had the hospital call him and he returned to deal with the situation. I presented a long-held question: “On 27 August, when he fell into severe shock, the term ‘cardiac tamponade’ never came up. Isn’t the only reasonable interpretation that cardiac tamponade was missed? Was this a missed diagnosis?” The doctor denied this, stating, “It was not missed.” When I asked, “If it wasn’t missed, then why did you not explain such an important matter to us?” he repeatedly gave inconsistent answers such as “There was no time to explain” and “It was a lack of explanation.” - 12 September: My father’s death, suspicious comments from the police officer, and the move to a “judicial autopsy”
During whole-body CT scanning (head, chest and abdomen), he went into cardiopulmonary arrest. Resuscitation was not initiated immediately and the CT scan was prioritized; there was a nine-minute gap before resuscitation was started. He was pronounced dead (acute subdural hematoma, suspicious death).
The hospital initially proposed a clinical autopsy, but we, the family, requested a judicial autopsy. We were told: “Whether it becomes a judicial autopsy will depend on the results of a postmortem examination by the police, who will decide if there is any suspicion of a criminal case. Shall we contact the police for you?” and we entrusted the calling of the police to the hospital (we, the family, did not directly confirm that the hospital actually contacted the police).
A man who identified himself as “○○, Chief of Criminal Division, Toride Police Station, Ibaraki Prefecture” (hereafter “Officer ○○”) entered the consultation room. “I am a neutral third party, so I cannot just listen to the family’s side,” he said, distancing himself from us, and when we tried to explain, he said, “I have trouble hearing such things from a layperson,” refusing to listen. He also said, “If you are a medical student and have medical knowledge, you could perform the autopsy yourself,” to which I replied, “No, I’m still a student and I don’t have that kind of authority.” He then continued, “Exactly. Even if you have knowledge, you don’t have the qualifications. So you have no choice but to ask a qualified doctor to do it. Do you understand?” speaking one-sidedly.
After that, he left the consultation room saying, “I will perform a postmortem examination,” and, after some time, returned and reported, “As a result of the postmortem examination, a judicial autopsy will be performed.”
He then asked a strange question: “This may sound odd, but roughly how much was your late father’s life insurance amount? It does not have to be exact.” We answered truthfully, “I think it was around 1 million yen,” but we still do not understand the purpose of that question.
Around 10:30 p.m., we saw my father’s body off at the back entrance of the hospital. “Officer ○○” urged us, saying “Please excuse your family members from here,” effectively sending us away, and we went home. At that point, my father’s body was surrounded by Officer ○○ and several cardiology doctors from the hospital. We, the family, did not witness what happened afterward, so we do not know where his body was taken or what was actually done.
Issues Extracted from Charts and Medical Records and Their Supporting Evidence
- 24 August: Attempt via right radial artery approach failed, switched to right femoral artery
PCI began at 22:35. The right radial artery was punctured and the procedure started, but the approach to the coronary artery failed and they restarted the procedure via the right femoral artery.
Evidence: The report includes the note “Right ra approach failed, changed”. “ra” refers to radial artery.
- 24 August: Suspicion that images of the major accident were removed
Video recording started at 23:02 (there is a 27-minute blank from the start of PCI to the start of video recording). There is no video documenting the failed approach to the coronary artery via the right radial artery at the beginning of the procedure. There is a possibility that the video of a major accident was removed.
Evidence: In the PCI video file list, the first file has a last-modified time of 23:02, and no video exists for the preceding 27 minutes.
- 24–25 August: Major procedural accidents (coronary injury, occlusion, perforation)
There is evidence of perforation of the left anterior descending artery, dissection and occlusion of the left main coronary artery, and suspected aortic injury.
Evidence: Extracts from PCI videos
For life-saving, an emergency open-chest operation in cardiovascular surgery would have been necessary, but the doctors did not arrange this. Instead, they left the situation as it was and were chatting after the procedure. - 24–25 August: Excessive radiation dose
According to the cardiac catheterization record, the radiation dose during PCI reached 10,350 mGy, far exceeding typical allowable limits.
Evidence: PCI report
- 26 August: Blood transfusion started when Hb was 11.1 g/dL
A blood transfusion was started because of anemia (noted in the chart and nursing records). However, the blood test that day showed Hb 11.1 g/dL, which indicates only mild anemia. If Hb 11.1 g/dL was accurate, transfusion was inappropriate; if transfusion was necessary, then the recorded Hb 11.1 g/dL may be inaccurate.
Evidence: Excerpts from chart, nursing records, and blood tests
- 27 August: APTT 92 seconds and heparin dose increased (suspicion of intentional hastening of death)
While shock due to bleeding into the pleural and/or pericardial spaces was progressing, a blood test on 27 August showed APTT 92 seconds, a panic value, yet the heparin dose was increased from 15,000 units to 20,000 units per day. This raises suspicion that death was deliberately hastened.
Evidence: Excerpts from blood test results and injection prescription sheets (highlighted in red)
- 27 August: Doctors and nurses recognized increasing pericardial effusion and the critical state
The chart for that day includes notes such as “pericardial effusion increasing” and “critical condition”.
Evidence: Chart entries
- 27 August: Use of a fictitious patient name, suggesting planned falsification
The ventilator setting record was written using the fictitious patient name “Tamaki Ishikawa”. This appears to be a record created on the assumption that it would later be destroyed.
Evidence: Ventilator setting record bearing the fictitious name
- Just after midnight on 28 August: Notes of “cardiac tamponade” and “pericardiocentesis”
It was recorded that echocardiography showed increased pericardial effusion, blood pressure fell to 50 mmHg, and pericardiocentesis was performed.
Evidence: Chart entries and explanatory sheet for the family
- 25–28 August: Oliguria/anuria and critical shock state
25 August: urine volume 779 ml/day; 26 August 21:30 – 27 August 5:30: urine volume 28 ml; 27 August 5:30–13:30: 15 ml; 13:30–21:30: 4 ml; 21:30 – 28 August 5:30: 144 ml (anuria due to shock, then increased urine volume as shock resolved).
Evidence: CCU nursing records (urine volume)
- Insurance claim for August 2010: No item for “pericardial fluid”
In the insurance claim for August 2010, there is no test item for “pericardial fluid”, only “pleural effusion”. → This suggests the possibility that the explanation of “pericardiocentesis” given by the doctor was inaccurate or incomplete.
Evidence: Extracts from the August 2010 insurance claim
- Life insurance certificate: No entry for pericardiocentesis
In the section for procedures, there is no description of pericardiocentesis.
Evidence: Extracts from the life insurance certificate
- 24–31 August: Severe shock liver and shock kidney
Liver function tests (AST, ALT) and renal function tests (creatinine) rapidly worsened in line with shock. Peak liver function values on 28 August were AST 4,018 U/L and ALT 3,177 U/L, indicating severe hepatic failure consistent with shock liver. Kidney function deteriorated with creatinine rising from 0.82 mg/dL (26 August) to 2.66 mg/dL (27 August) and 5.15 mg/dL (28 August), consistent with shock kidney.
Evidence: Blood test data
- 12 September: Evidence of hemothorax and tension hemothorax
Chest X-ray and CT showed widened mediastinum and pleural effusion. Anemia severe enough to require transfusion cannot be explained by pericardial bleeding alone.
Evidence: Thoracoabdominal CT showing hemothorax
- 12 September: Acute subdural hematoma
Head CT performed on the day of death showed a severe acute subdural hematoma. According to the doctor, “The cause was a bleeding tendency due to DIC,” with no explanation of head trauma.
Evidence: Head CT showing acute subdural hematoma
- 12 September: Only mild bleeding tendency
PT-INR 1.3, APTT 35 sec, platelets 36,000/μL, Hb 8.2 g/dL: the bleeding tendency was only mild, making spontaneous onset of a subdural hematoma highly unlikely. At this time, my father was unconscious and unable to move by himself, leaving external head trauma as the only plausible mechanism.
Evidence: Blood test data (12 September)
Summary of Analysis and Verification of the In-Hospital Course and Medical Records
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24 August 2010, my father developed myocardial infarction and was transported to Toride Kyodo Hospital in Toride City, Ibaraki Prefecture.
He was diagnosed with acute myocardial infarction, and emergency PCI (percutaneous coronary intervention) was performed in the cardiology department.
The procedure started at 22:35, with a guidewire inserted into the right radial artery. However, they failed to advance into the coronary artery and switched to insertion via the right femoral artery. During this period, there is no PCI imaging for the time when the initial approach failed, raising the possibility that images documenting a major accident were removed. PCI took three hours, and the radiation dose during that period was extremely high, enough to have a serious impact on the human body. Reviewing the PCI videos shows left main coronary artery occlusion, damage and dissection, perforation of the proximal and distal segments of the left anterior descending artery, and thrombotic occlusion of the left circumflex branch—multiple severe technical errors. To save his life, emergency open-chest surgery in cardiovascular surgery would have been necessary, but after PCI, the doctors told the family “The treatment was successfully completed,” concealed these technical errors, did not arrange for cardiovascular surgery, and instead were chatting casually.
As an inevitable result, bleeding into the pleural and pericardial spaces occurred, with tension hemothorax, cardiac tamponade, and hemorrhagic shock progressing until he became critically ill.
At around 3:00 p.m. on 27 August, his blood pressure was 60/40 mmHg, heart rate 150–160/min, and urine output in the preceding eight hours was only 4 ml—conditions under which cardiopulmonary arrest could occur at any moment. However, the doctor falsely explained that the cause of shock was “because the original myocardial infarction was severe,” thereby concealing both the medical accident and the resulting tension hemothorax, cardiac tamponade, and hemorrhagic shock. Furthermore, although heparin was being administered at 15,000 units/day and his APTT that day was 92 seconds—indicating an excessive heparin effect—the dose was increased to 20,000 units/day, raising suspicion that there was intent to hasten his death.
After midnight on 28 August, he was taken out of shock, but his family was neither contacted nor asked for consent. There are no call records to our phones. When I became worried and went to the hospital, at 9:30 a.m. on 28 August his blood pressure was 110/60 mmHg and heart rate 100/min, showing he had been taken out of shock. The doctor explained, “During the night his blood pressure dropped further, so we performed echocardiography and found that pericardial effusion had accumulated and he had developed cardiac tamponade, so we performed pericardiocentesis.” He added, “The cause is called oozing-type ventricular rupture, in which blood slowly leaks into the pericardial sac through gaps in infarcted and fragile myocardium, and in any case it is a dangerous condition.”
Regarding this resolution of shock, the doctor explained it as “pericardiocentesis”, and the chart also records “pericardiocentesis”. However, the life insurance certificate has no entry for “pericardiocentesis” in the procedure section, and the insurance claim lists “pleural effusion” rather than “pericardial fluid”, meaning there are discrepancies among the records. It is difficult to imagine that pericardial bleeding alone would cause anemia severe enough to require transfusion; bleeding into a larger space (the pleural cavity) must have been present. In fact, if we interpret the procedure as “pleural effusion drainage”, the need for transfusion and the high likelihood of hemorrhagic shock fit seamlessly with the clinical course. This makes it highly likely that the actual condition was tension hemothorax and hemorrhagic shock due to intrathoracic bleeding, and that the procedure performed to reverse shock was pleural effusion drainage.
From admission on 25 August through 28 August, liver function values (AST, ALT) and renal function values (creatinine) rose sharply on blood tests. Peak values on 28 August—AST 4,018 U/L and ALT 3,177 U/L—indicate severe hepatic failure; the course strongly suggests shock liver. Creatinine rose from 0.82 mg/dL on 26 August to 2.66 mg/dL on 27 August and 5.15 mg/dL on 28 August, indicating rapid day-by-day deterioration of renal function, congruent with the course of hypotension, and consistent with shock kidney.
Because shock persisted for a prolonged period, multiple organs—including the liver and kidneys—were severely damaged, leading to multi-organ failure and an irreversible condition.
On 5 September the sedatives were discontinued, but my father did not regain consciousness. The attending physician said only that “Because his liver function is poor, the sedatives may be taking longer than usual to clear,” and “He may have had a stroke,” offering only vague “maybes”. However, from a unified medical perspective, the most reasonable interpretation is hypoxic encephalopathy due to decreased cerebral blood flow during severe shock.
On 12 September, when his condition deteriorated, head and thoracoabdominal CT were performed. According to the doctor’s explanation and the chart, the stated purpose of the CT was “to investigate the source of bleeding because anemia had progressed.” However, it is uncommon for head bleeding to cause progressive anemia, and if the purpose were to search for the bleeding source, thoracoabdominal CT alone would generally be sufficient. From a medical standpoint, the real purpose of these CT scans appears to have been postmortem imaging (autopsy imaging) to determine the cause of death.
The head CT taken at that time showed an acute subdural hematoma, which became the direct cause of my father’s death. The doctor explained this, but there was no mention at all of “head trauma”, which would ordinarily be considered the direct cause (this is confirmed by audio recordings). Instead, he attributed it to “spontaneous bleeding due to the bleeding tendency accompanying DIC (disseminated intravascular coagulation).” However, blood tests performed almost simultaneously showed “PT-INR 1.3, APTT 35 sec, platelets 36,000/μL,” indicating only mild bleeding tendency. Under such conditions, spontaneous intracranial bleeding is extremely unlikely.
From this, the cause of the acute subdural hematoma that directly caused his death can be determined to be head trauma. At that time my father was unconscious and unable to move on his own, so it is reasonable to infer that the head trauma was caused by external force. In other words, his death was suspicious and should have been treated as such.
Even without the subdural hematoma, my father’s condition was irrecoverable, and he was in a state where he would eventually have died from his underlying condition. From the medical records and course, the conclusion that inevitably emerges is that there was deliberate neglect to bury the medical accident in darkness, followed by head trauma to hasten his death.
The thoracoabdominal CT taken at the same time also showed a crescent-shaped hematoma-like lesion around the aorta and multiple residual clotted blood masses in both pleural cavities, which appear to be organized (fibrotic) blood clots. These findings are evidence of bleeding from the aorta into the pleural cavity due to aortic injury, and they preserve traces of the initial medical accident during PCI.
Change of Hospital Name (Toride Kyodo Hospital → JA Toride General Medical Center)
※ This hospital (Toride Kyodo Hospital) changed its name to “JA Toride General Medical Center” on 1 April 2011, at the start of the new fiscal year following this major incident.Links to Primary Materials
- Analysis of chart entries
- Extracts from medical records (1)
- Clinical course and physician explanations
※ Redacted versions for public release will be placed at each link. They can be verified against the original documents using SHA-256 hashes.