Fatal thrombosis of the basilar artery due to a minor head injury

A case is reported where a 20-year-old alcohol-intoxicated man was admitted to the hospital after a minor head injury. Initially there was no neurologic disturbances or complaints but after a few hours he became comatose, and he died 4 days later without regaining consciousness. The autopsy revealed no lesions of the upper cervical spine or the vertebral arteries, but the basilar artery was occluded in its entire length. No traumatic lesions could be seen by naked eye examination of the artery, and there was no accompanying subarachnoid haemorrhage. A thorough microscopic examination, however, using step-sectioning technique revealed a significant incomplete arterial rupture with an occluding luminal thrombosis superimposed, consisting predominantly of aggregated platelets. Only the very thin adventitia separated the vascular lumen from the subarachnoid space preventing the more well known fatal complication to a minor head injury: A subarachnoid haemorrhage. To the best of our knowledge, fatal thrombosis of the basilar artery due to a minor head injury has not previously been reported. The pathogenetic mechanism seems to be identical to that underlying fatal subarachnoid haemorrhage following a similar trauma apart from the resulting arterial rupture being incomplete instead of complete.     

Fatal dissecting aneurysm of the internal carotid artery with delayed symptoms following facial impact.

A fatal dissecting aneurysm of the internal carotid artery occurred in a 16-year-old male following facial impact in an automobile accident. The patient showed no neurologic deficit until two days after the automobile accident, when he suddenly started having seizures and developed right-sided hemiparesis. There was no evidence of direct trauma to the neck externally or internally. The only injuries observed in the head and face were two skin lacerations in the chin area. His condition rapidly deteriorated, and he expired on the fourth hospital day. The gross and microscopic findings for the internal carotid artery are presented. The possible mechanisms for the vascular lesion and a review of the literature are discussed.     

Cerebral infarct following traumatic carotid artery thrombosis

An autopsy case of a 45-year-old man is presented. The man had sustained a minor head injury in a traffic accident 11 years ago previously and 5 years later had a cerebral infarction due to thrombosis of the carotid artery. There was histological evidence of a traumatic lesion of the vessel wall. Several contradictory expert opinions were rendered regarding the questionable causal relationship between occlusion of the artery and the previous trauma. In the court of appeal, an agreement was arrived at between the widow of the deceased and the third-party insurance of the person responsible for the accident.     

Fatal blunt trauma of the larynx in a child

We report an autopsy case of an 11-year-old girl who suffered mechanical asphyxia from falling off the metal bars in the playground. This autopsy case is interesting because of the atypical trauma and lesions. To our knowledge there has been no similiar published case reports in the forensic literature. The young age of the victim, the setting and the pattern of the injuries are rare in a fall at playground by a child.     

Cardiac rupture following blunt trauma

A case of cardiac rupture following blunt trauma with no additional injuries is described. This can be a difficult diagnosis because of the presence of additional injuries and the lack of clinical symptoms. Here, there was a rupture of the pericardium, all chambers of the heart and the thoracic aorta.     

Fatal trauma to the neck: immunohistochemical study of local injuries

As fatal trauma to the neck is often associated with short survival times, proof of vitality may often be difficult using standard histochemical techniques. Soft tissue neck injuries resulting from strangulation by ligature or manual strangulation were examined immunohistochemically using antibodies to myoglobin, fibronectin, C5b-9 and MRP14, and compared to controls consisting of accidental soft tissue neck injuries as well as undamaged neck soft tissue. Although survival times in the study and control groups were unknown and certainly some individual variation may be expected in the time course of normal wound development, both the study and control groups demonstrated similar time courses in the immunohistochemical detection of antigen. Myoglobin was always found in those samples in which only one antigen was shown to be involved in an injury-specific pattern; myoglobin and fibronectin were found in samples with dual antigen involvement. Samples involving three antigens always included C5b-9 in addition to myoglobin and fibronectin. The single positive MRP14 sample in the study and control groups was simultaneously positive for the other markers used. Myoglobin, fibronectin, C5b-9 and MRP14 are therefore suitable for immunohistochemical detection of vital reactions and estimation of temporal relationships in the early posttraumatic period after neck trauma.     

Seat-belt injuries to the left common carotid artery and left internal carotid artery

Seat-belt injuries to the neck in a traffic accident or any trauma to the neck in other situations can cause tearing of the inner surface of the carotid arteries and lead to the formation of a fresh thrombus, or can cause partial to complete transection of the carotid arteries.     

Spinal epidural haematoma after blunt trauma to the neck and hyperflection of the cervical spine

Spinal epidural haematomas (sEDH) can be regarded as rare events, in principle a spontaneous and a traumatic aetiology can be distinguished. Spontaneous spinal epidural haematomas can arise, e.g. from vascular malformations, coagulopathies, etc. On the other hand, traumatic sEDH are related to, e.g. spinal trauma or intraoperative vascular injuries. With regard to clinical significance, spinal epidural haematomas accompanied by transient mild neurological symptoms up to lethal outcomes have been observed. We report on a 53-year-old male alcoholic who was found in the kitchen of his asylum in a grotesquely fixed body position, with his head and cervical spine in a maximum anteflected position. A general practitioner had ruled for a non-natural manner of death due to "broken neck" and alcohol intoxication, therefore, the prosecution authorities called for a medicolegal autopsy. At autopsy, paravertebral soft tissue haemorrhage in between the shoulder blades was disclosed. Furthermore, a spinal epidural haematoma, extending from the foramen magnum down to the middle portion of the thoracic spine was found. No fractures of vertebrae nor lesions of spine ligaments or bleedings of intervertebral discs were found. Blood alcohol concentration was determined 1.92 g/l and urine alcohol concentration was 1.76 g/l. Further morphological findings were cerebral oedema and cardiac hypertrophy; the urinary bladder was found filled to bursting. Neuropathological investigations confirmed the presence of the spinal epidural haematoma and assigned lethal significance to this finding. There were no histological signs of axonal injury. Reconstruction revealed that when sitting on a chair in a drunk condition, the individual's upper part of the body had fallen backwards in the corner and subsequently got stuck with maximum anteflection of the head and cervical spine, causing rupture of vessels and spinal epidural haematoma. Acute respiratory failure caused by impairment of the phrenic nerve following spinal epidural haematoma with potential synergism of alcohol intoxication was ascertained as the cause of death.     

颈动脉钝性损伤法医学研究进展

颈动脉钝性损伤的发生率虽低,但死亡率高,易发生于交通事故、扼勒、缢吊、颈部直接外力作用和高坠等案例中。颈动脉钝性损伤有5种基础成伤机制：颈部直接外力作用,颈部过度伸展和旋转,颅底骨折碎片切割,口腔内扁桃体窝处直接外力作用,头胸部复合伤造成颈动脉被牵拉。国外相关研究文献和个案报道较多,而国内未见系统研究,不多的个案报道中,也有错误鉴定案例。本文对颈动脉钝性损伤的致伤方式、解剖学和生物学基础、成伤机制和法医学鉴定注意事项进行综述,希望能引起国内法医技术人员的重视,并为相关研究和应用提供参考。     

Further investigations into the speed of cerebral swelling following blunt cranial trauma

An anesthetized sheep model of traumatic brain injury (TBI) has been developed to assess early changes in intracranial pressure (ICP) following closed head injury. Immediately after TBI, a transient (<10 min) hypertensive response occurred, followed by significant and prolonged systemic hypotension. ICP demonstrated a biphasic response, being seven times baseline values of 8 ± 2 mm Hg 10 min after injury, decreasing to 25 ± 2 mm Hg by 30 min, and then increasing to values exceeding 30 mm Hg by 4 h postinjury. ICP was always significantly higher than baseline values, which combined with hypotension, reduced cerebral perfusion pressure to less than 60% of normal. This early and sustained increase in ICP after craniocerebral trauma acutely alters cerebral perfusion pressure and brain oxygenation and provides a potential pathophysiological explanation for immediate clinical manifestations in humans following significant TBI.     

Sudden death due to delayed rupture of hepatic subcapsular hematoma following blunt abdominal trauma

Blunt abdominal trauma can cause sudden, unexpected death due to injuries to internal organs. Rupture of a hepatic subcapsular hematoma is a relatively rare cause of sudden death following minor blunt abdominal trauma. Death may be delayed several days to weeks. The autopsy is an invaluable diagnostic tool that can be utilized to uncover sudden deaths due to abdominal trauma. The case of an alcoholic who died of a ruptured hepatic subcapsular hematoma is presented. The death investigation revealed that the victim had sustained blunt abdominal trauma during a fall a few days prior to death.     

Fatal and non-fatal bilateral delayed carotid artery dissection after manual strangulation

Carotid artery (CA) dissection and/or thrombosis may occur in a number of medical and forensic relevant situations. However, post traumatic carotid artery dissection is considered rare, and often underestimated due to possible delayed presentation. We describe two cases of carotid artery dissection following strangulation with delayed symptoms as well as discuss medical diagnostic problems and their forensic implications.     

Azygos vein laceration due to blunt trauma

The azygos vein ascends along the thoracic spine through the mediastinum and drains into the superior vena cava at the level of the fourth thoracic vertebra. Fracture-dislocation of the mid-thoracic spine, as a result of blunt thoracic trauma, can tear the azygos vein. Four such fatal cases (three motor vehicle accidents and one fall) were studied, only one of which was recognized prior to death. The vein can also be torn, in the absence of skeletal injuries, by horizontal acceleration/deceleration forces. The pathologist must consider azygos vein laceration as a possible cause of either hemothorax or hemomediastinum or both in a victim of a blunt chest trauma, if that individual had persistent hypotension during the few hours before death and no identifiable source of hemorrhage can be found postmortem in sites such as the heart, great vessels, lung, and chest wall. A fracture-dislocation of the thoracic spine may not necessarily be present. Azygos vein laceration seems to be an uncommon cause of hemothorax and hemomediastinum; however, this injury is probably more frequent than is implied by the few cases described in the medical literature.     

Delayed cardiac rupture due to blunt chest trauma

A 7-year-old boy fell from a 2.5-m height and suffered contusion of the thorax with hematoma in the soft tissues of the lateral chest wall. The rib cage itself remained intact. After 3 days, there was only local pressure sensitivity of the left hemithorax. On day 8 after the trauma, the child, who up to then had seemed to be in good health, suddenly died during lessons at school. Autopsy revealed a full-thickness rupture of the left ventricle with resultant cardiac tamponade. The macroscopic and histopathologic findings are presented and discussed.     

Occlusion of left and right coronary arteries and coronary sinus following blunt chest trauma

Blunt chest trauma from rapid automobile airbag deployment causing coronary artery occlusion and myocardial infarction is a rare but potentially fatal condition. We present the case of a 37-year-old man who developed extensive anterior and inferior myocardial infarction because of occlusion of both left anterior and right coronary arteries following blunt injury to the chest in a car accident. The patient was scheduled for emergency coronary angiography but left and right coronary ostia were not cannulated because of thrombus formation probably. The patient died, and the autopsy revealed external compression by epicardial hematomas involving separately left and right coronary arteries and the coronary sinus without signs of coronary and/or aortic dissection. To our knowledge, this is the first case presenting occlusion of both coronary arteries secondary to blunt chest trauma causing acute myocardial infarction in a young man without signs of prior coronary artery disease.     

Taphonomic changes to blunt force trauma: a preliminary study

This study examines the effects of taphonomic processes on blunt force trauma (BFT) through an experimental study involving pig heads. Of particular concern is the possibility that taphonomic changes can create pseudo-trauma and/or conceal evidence of actual trauma. BFT was inflicted on 10 pig skulls using a hammer. The skulls were subsequently exposed to the environment for 12 months. Seven taphonomic changes were evaluated: the freeze-thaw cycle; rodent gnawing; carnivore scavenging; presence/weight of soil; presence/weight of rain and snow; movement/displacement of bones; and discoloration due to sun bleaching and grass staining. Taphonomic effects varied between cancellous, compact, fresh, and degreased bone. Freezing and thawing, exposure to rain and snow, movement of the skulls, and soil erosion altered and, in some cases disguised, pre-existing trauma. Rodent and carnivore activity did not obliterate evidence of BFT. Recommendations for evaluating BFT on remains affected by taphonomic processes are presented. As each taphonomic process outlined by this study has the potential to disguise antemortem injury, the authors propose that one must carefully examine large, circular openings in the skull that may represent the remnant evidence of BFT.     

Rapidly growing internal carotid artery aneurysm after amphetamine abuse: case report

Amphetamine is one of the most common illicitly abused drugs in certain countries. It is a potent sympathomimetic that may lead to vascular events, including stroke and myocardial infarction. Most reports of stroke after amphetamine abuse are of intracerebral hemorrhage. In this report, the authors describe a ruptured aneurysm of the right internal carotid artery in a young man with amphetamine abuse. It grew rapidly within 2 weeks. Surgery revealed fibrosis and fibrinoid necrosis around the aneurysm. The aneurysm was successfully embolized with Guglielmi detachable coil. A rapidly growing aneurysm in the major intracranial vessels resulting from amphetamine abuse is very rare.     

Necrotizing fasciitis: a fatal outcome following minor trauma. Case report and literature review

The death of a young healthy man, 11 days after he sustained minor trauma, illustrates the potential disaster of undiagnosed necrotizing fasciitis. Difficulty in early diagnosis often arises because the skin is initially spared and only later becomes secondarily involved. In this case, because of the lack of external manifestations, the diagnosis of necrotizing fasciitis was not considered until the postmortem examination. Necrotizing fasciitis should be considered a potentially serious problem that can follow minor trauma and eventually lead to death. The need for a high index of suspicion to make this diagnosis, along with the medicolegal implication of a diagnosis of necrotizing fasciitis, are both addressed in this report. Also of note is the fact that this patient was treated with nonsteroidal antiinflammatory drugs for pain and inflammation, which has recently been reported to be associated with an increased incidence of fulminant evolution of necrotizing fasciitis.     

Homicidal death following blunt trauma in a vulnerable host, with secondary infections including local tetanus

An uncommon type of homicide resulted from complications of an ordinarily nonfatal injury after a 59-year-old obese, hypertensive, diabetic man was struck in the face with a two-by-four, sustaining a grossly contaminated laceration. It was cleaned and sutured primarily, and a tetanus booster was given. On the fourth hospital day there was evidence of anerobic wound cellulitis, including Clostridium tetani. The wound was surgically debrided, but 2 days later the patient developed local tetanus. Only then was it discovered that he had never been immunized against tetanus. He did not develop systemic tetanus, but 2 days later he died with bronchopneumonia and sepsis. The assailant was indicted for involuntary manslaughter, but after a contentious trial he pleaded "no contest" to a reduced charge. The decedent was a vulnerable host, his contaminated facial laceration initiating an unbroken course of events that led to his death.