Independent Case Archive – An Unresolved Case in Which a Patient’s Unnatural Death Was Erased Through Coordinated Actions by Relevant Institutions (Japan)

This page summarizes, from a medical perspective, the in-hospital course of the patient at a regional hospital in Ibaraki Prefecture, Japan, from 24 August 2010 (onset of acute myocardial infarction and PCI) to 12 September 2010 (death due to acute subdural hematoma and suspected hemothorax), based on hospital records, imaging, laboratory data, and contemporaneous explanations documented by the family.

Case Definition (for independent review)

This archive documents an unprecedented unresolved case in Japan in which the unnatural death of a patient that occurred inside a hospital was jointly erased by relevant institutions and treated as if it had never existed. The materials indicate that medical procedures were carried out without an intent to treat the patient and that the clinical course was deliberately directed toward death. Following the death, the hospital, police, and administrative authorities acted in coordination to substitute the cause of death from an unnatural death to a natural death, thereby eliminating the incident from official records and effectively erasing its existence.

This case concerns a death following medical intervention in Japan that presents indicators of intentional lethal acts within a hospital setting, rather than an accidental medical error. The central issue is not the fatal outcome itself, but a sequence of actions in which treatment was not pursued in good faith, life-saving options were withheld, and the clinical course was steered toward death. After death, circumstances warranting independent scrutiny appear to have been systematically reclassified as natural causes through coordinated medical representations, post-mortem mischaracterization, and administrative processing. Taken together, the materials raise serious questions about the failure—and possible subversion—of medical, forensic, and oversight safeguards intended to prevent such outcomes.

Key medical issues addressed on this page:

Whether the PCI was technically successful or caused major iatrogenic injury.
Whether shock and multi-organ failure were due only to the infarction, or to procedure-related bleeding.
Whether “pericardiocentesis” was accurately documented, or whether tension hemothorax was the true problem.
Whether the acute subdural hematoma on 12 September 2010 can be explained by coagulopathy alone.

1. Brief Clinical Course (24 Aug – 12 Sep 2010)

24 August 2010 – Acute MI and PCI

Patient develops acute myocardial infarction and is transported to the hospital.
Emergency PCI is started at 22:35.
Initial access via right radial artery fails; the procedure is restarted via the right femoral artery.
The PCI lasts around three hours; radiation dose reportedly reaches approximately 10,350 mGy, well above typical thresholds for a single procedure.
After the procedure, the attending physician tells the family that “the procedure was successful, but the original infarction was severe, so the course may be difficult.”
The patient is conscious and expresses relief and gratitude; the atmosphere among staff appears relaxed.

25 August 2010 – Persistent Hypotension

Despite multiple vasopressors, blood pressure remains low and heart rate is elevated.
The patient is still conscious. Physicians describe the situation as “severe.”

26 August 2010 – Clinical Deterioration, Transfusion, Intubation

Emergency call to the family: “The situation is getting worse. Do you wish for aggressive treatment?” – the family answers “Of course, yes.”
Transfusion is started for “anemia,” but the same-day lab reports hemoglobin 11.1 g/dL, only mild anemia.
Endotracheal intubation and mechanical ventilation are initiated.

27 August 2010 – Profound Shock

By approximately 15:00: blood pressure 60/40 mmHg, heart rate 150–160/min.
Extremely low urine output (e.g., only 4 mL over an 8-hour interval at one point), consistent with severe shock and acute kidney injury.
Physicians tell the family there are “no remaining options” and that death is likely within hours.

28 August 2010 – “Pericardiocentesis” and Partial Recovery

The next morning, vital signs are improved (BP around 110/60 mmHg, HR ~100/min).
Only at this stage, the attending physician reports that during the night the patient developed cardiac tamponade and that “pericardiocentesis” was performed emergently.
No prior phone call or consent was obtained from the family, and there is no evidence of attempted contact.

5–9 September 2010 – Persistent Coma after Weaning

5 September: sedative medications are discontinued.
9 September: the patient is extubated and weaned from mechanical ventilation, but consciousness does not return.
Physicians suggest possibilities such as “delayed clearance of sedatives due to liver dysfunction” or “possible cerebral infarction,” but do not emphasize hypoxic-ischemic brain injury due to prolonged shock.

11–12 September 2010 – Final Deterioration and Death

11 September: the patient remains unresponsive; the face appears distressed. The on-duty physician has gone home; he is called back, and the family raises the long-standing question of missed tamponade.
12 September: head and chest–abdominal CT are performed. During CT, the patient experiences cardiopulmonary arrest. There is a reported 9-minute period during which CT imaging is prioritized over resuscitation.
Head CT shows a large acute subdural hematoma. Chest–abdominal CT shows findings compatible with hemothorax and para-aortic hematoma.
Blood tests show only mild coagulopathy and thrombocytopenia, insufficient to explain a spontaneous massive subdural hematoma in an immobile, unconscious patient.
The patient is pronounced dead. The formal cause of death is later attributed to disease, not trauma.

2. PCI Procedure: Evidence of Major Iatrogenic Injury

Based on the PCI records and videos preserved through court-ordered evidence, several technical and radiological features suggest that the PCI was not “uneventful” but was associated with severe iatrogenic damage.
　　:contentReference:PCI record, PCI report, PCI videos

2.1 Missing Early PCI Images

The recorded video files begin at 23:02PCI time table – 27 minutes after the documented start of PCI at 22:35.PCI record
There are no images from the period when access was attempted via the radial artery and then changed to femoral access.
The absence of these images raises the concern that crucial footage documenting a serious complication was removed.

2.2 Suspected Lesions on the PCI Videos

Review of the PCI imagesPCI video indicates:
- Dissection and occlusion of the left main coronary artery.
- Perforation of the proximal and distal segments of the left anterior descending artery.
- Evidence of aortic injury and possible thrombotic occlusion in the left circumflex territory.
In such a situation, standard of care would typically require urgent surgical consultation and possible emergent open-heart surgery (e.g., repair of perforation, control of bleeding).
According to the family’s account and the chart, no such transfer or surgical intervention was arranged; instead, the procedure was later described to the family as “successful.”
　　:contentReference:PCI Report（COLONARY REPORT）}

2.3 Excessive Radiation Dose

The catheterization record documents a radiation dose around 10,350 mGy during PCIPCI Report（COLONARY REPORT） – far above typical doses for coronary intervention.
This level suggests prolonged fluoroscopy and repeated contrast injections, consistent with a technically difficult and complicated procedure.

3. Shock, Hemodynamic Instability, and Organ Failure

From 25–28 August, the patient shows a pattern of progressive shock, multi-organ failure, and then partial hemodynamic recovery. The laboratory data and nursing records provide an objective picture of this course.
　　:contentReference:CCU_Nurse_Record, laboratory data summary, laboratory data raw

3.1 Hemodynamic Course and Urine Output

Persistent hypotension despite vasopressors, with tachycardia in the range of 150–160/min on 27 August.CCU_Nurse_Record
Urine output falls from 779 mL/day on 25 August to as low as 4 mL over an 8-hour period on 27 August, indicating severe renal hypoperfusion and shock.CCU_Nurse_Record
After the nocturnal procedure on 28 August (described as “pericardiocentesis”), urine output increases, consistent with relief of shock.CCU_Nurse_Record

3.2 Liver and Kidney Dysfunction (Shock Liver and Shock Kidney)

Liver enzymes rise dramatically:
- AST peak around 4,018 U/L, ALT peak around 3,177 U/L (consistent with severe “shock liver”).laboratory data summary, laboratory data raw
Serum creatinine increases rapidly from normal (around 0.82 mg/dL) to approximately 5.15 mg/dL within a few days, consistent with acute renal failure (“shock kidney”).laboratory data summary, laboratory data raw
After shock is relieved, no further marked worsening is recorded, supporting the interpretation that organ failure was shock-induced rather than due to primary hepatic or renal disease.laboratory data summary, laboratory data raw

3.3 Anticoagulation and APTT 92 Seconds

On 27 August, while the patient is in ongoing shock with suspected internal bleeding, APTT is recorded as 92 seconds – a panic-level prolongation under heparin therapy.laboratory data 8/27
Despite this, the heparin dose is increased from 15,000 units/day to 20,000 units/day, which is difficult to justify medically and raises concern that the bleeding risk was knowingly exacerbated.heparin 20000(8/27)

3.4 Anemia and Transfusion

Transfusion is initiated on 26 August for “anemia,”(transfusion) yet the same-day hemoglobin is documented at 11.1 g/dL (mild anemia).(laboratory data 8/26)
If 11.1 g/dL is accurate, transfusion would be questionable; if transfusion was clinically necessary, the recorded value may be unreliable.
In either case, the records around anemia, bleeding, and transfusion are internally inconsistent.

4. Cardiac Tamponade vs. Tension Hemothorax

The official explanation for the shock episode and its resolution is “cardiac tamponade due to oozing-type myocardial rupture, treated by pericardiocentesis.”cardiac tamponade and pericardiocentesis However, multiple documents suggest that the actual pathophysiology was more consistent with massive bleeding into the pleural space (tension hemothorax) and possibly para-aortic hemorrhage.

4.1 Inconsistent Documentation of Pericardiocentesis

Physician’s note and explanation to the family refer to “pericardiocentesis for cardiac tamponade.”cardiac tamponade and pericardiocentesis
However:
- The insurance claim (life insurance medical certificate) does not list pericardiocentesis among the procedures.(life insurance certificate)
- The billing/claims (receipt) for August 2010 list “pleural fluid” but not “pericardial effusion,” suggesting that pleural, not pericardial, drainage was coded.(receipt(August 2010))
These discrepancies raise doubt as to whether the procedure was truly pericardiocentesis, or instead a pleural drainage for hemothorax.

4.2 Hemodynamic and Hematologic Context

The patient requires transfusions and exhibits progressive anemia that cannot be fully explained by pericardial bleeding alone.
Massive pericardial bleeding sufficient to require transfusion would almost certainly be associated with a large hemopericardium; yet the billing and some records emphasize “pleural effusion.”
From a physiological standpoint, a large-volume hemothorax with mediastinal shift (tension hemothorax) is more consistent with the clinical picture and the subsequent CT findings.

4.3 Later CT Evidence

On 12 September, chest CT(chest abd CT 2010/9/12) shows:
- Para-aortic crescent-shaped high-density collection consistent with hematoma.
- Bilateral pleural collections with residual clot-like material, compatible with prior hemothorax.
These findings strongly suggest bleeding from the aorta into the mediastinum and pleural space, likely related to the earlier PCI-induced vascular injury.

Taken together, the hospital’s narrative of “oozing-type myocardial rupture with tamponade treated by pericardiocentesis” does not reconcile well with the billing data, the need for transfusion, nor the CT evidence of para-aortic hematoma and hemothorax.

5. Neurological Outcome and Acute Subdural Hematoma

5.1 Persistent Coma after Shock

Despite discontinuation of sedatives and successful weaning from mechanical ventilation, the patient does not regain consciousness.
Given the documented period of severe shock (profound hypotension, multi-organ failure), hypoxic-ischemic brain injury is a highly plausible and medically coherent explanation.
However, this hypothesis is not emphasized in physician explanations; instead, speculative causes (“sedative accumulation,” “possible stroke”) are mentioned without clear diagnostic work-up.chart 2010/9/12-①

5.2 CT on 12 September: Acute Subdural Hematoma

Head CT on 12 September shows a large acute subdural hematoma, which becomes the immediate cause of death.(head CT 2010/9/12 )
Physicians attribute this to bleeding tendency due to DIC (disseminated intravascular coagulation), without any mention of head trauma.

5.3 Coagulation and Platelet Counts at the Time of Death

Near the time of death, blood tests show(laboratory data 2010/9/12):
- PT-INR 1.3
- APTT 35 seconds
- Platelet count ~36,000/µL
- Hemoglobin 8.2 g/dL
These values indicate mild coagulopathy and thrombocytopenia, but not the level of derangement typically associated with spontaneous massive subdural hematoma in an immobile patient.
The patient is unconscious and cannot move or fall independently; there is no documented accidental trauma.

Under these conditions, a spontaneous large acute subdural hematoma is medically implausible. The pattern is more consistent with external head injury (blunt trauma) in a patient with modestly impaired but not catastrophic coagulation. The hospital records, however, do not document any such trauma or investigate it.

6. Integrated Medical Interpretation (Summary)

Based on the medical records, imaging, and laboratory data summarized above, the following interpretation emerges:

PCI-related injury: The PCI appears to have caused major mechanical injury to the coronary arteries and possibly the aorta, as suggested by image-based evidence and the later CT findings.
Shock and multi-organ failure: The resulting bleeding into the thoracic cavity (and possibly pericardial space) led to prolonged shock, causing severe liver and kidney failure (“shock liver” and “shock kidney”) and likely hypoxic brain injury.
Tamponade vs. hemothorax: The documentation around “pericardiocentesis” is inconsistent with billing data and clinical context. The overall picture fits tension hemothorax and para-aortic bleeding better than isolated pericardial tamponade.
Subdural hematoma: The large acute subdural hematoma found on 12 September 2010, in the setting of only mild coagulopathy and an immobile unconscious patient, is unlikely to be spontaneous. It strongly suggests head trauma, which is neither documented nor explained.

From a medical standpoint, the hospital’s narrative—“severe primary infarction, difficult course, DIC-related bleeding”—does not adequately explain the full sequence of events. The objective data instead point toward:

a catastrophic PCI-related iatrogenic injury,
prolonged uncorrected shock with multi-organ failure, and
an unexplained traumatic acute subdural hematoma near the end of the hospitalization.

This page is a technical medical summary based solely on available records and imaging. Legal classification of the case (medical negligence, homicide, etc.) is discussed separately in the Legal Issues section.

7. Links to Primary Medical Evidence

The following materials (with identifying information redacted for public release) support the analysis above:

Original (non-redacted) files and cryptographic hashes can be provided to independent experts, courts, and human-rights bodies under appropriate confidentiality conditions.