scholarly journals Near-hanging with outliving period: Pathoforensic aspects

2012 ◽  
Vol 140 (3-4) ◽  
pp. 198-203
Author(s):  
Vladimir Zivkovic ◽  
Slobodan Nikolic

Introduction. Hanging usually ends in death, and about 80% of victims are found dead at the scene of the hanging. However, sometimes the hanging victims overlive for some time, and sometimes even survive the hanging. Objective. The aim was to determine the causes of death in nearhanging cases, in people who have been outliving hanging for some time, to explain the pathophysiological mechanisms leading to death, and to identify prognostic factors for this outcome. Methods. Retrospective autopsy study was performed for a twelve-year period. There were only seven cases of near hanging. The sample was analyzed according to gender, age, circumstances of death, and autopsy findings of all observed subjects. The relevant data were collected from autopsy records, police reports and heteroanamnestic interviews. Results. The sample consisted of five men and two women, average age 48.3?19.9 years (29-81 years). The average outliving period was 3.8?2.6 days (from 7 hours to 7 days). Six people were admitted to hospital in the state of deep coma. In six cases cardiopulmonary arrest occurred after the hanging attempt and all were reanimated for a shorter or longer time until admission at hospital. Conclusion. Survival after attempted suicide by hanging occurs extremely rarely. In all the cases, the immediate cause of death after attempted hanging was ischemic brain injury, with a significant and pronounced oedema. In all the cases observed, regardless of the presence or absence of injuries of soft and hard structures of the neck, there was a ligature mark on the neck skin. Acute hemorrhagic gastritis with melaena was present in a significant number of reported cases of near-hanging.

2021 ◽  
pp. 485-488
Author(s):  
Tia Chakraborty ◽  
Jennifer E. Fugate

Anoxic-ischemic brain injury occurs when no blood is flowing to the brain. Neurologists commonly encounter this clinical state when evaluating comatose patients who have had a cardiac arrest and prolonged cardiopulmonary resuscitation attempts. Anoxic-ischemic injury may also occur in primary respiratory arrest or severe hypoxemia (eg, asphyxia, anaphylaxis, drug intoxication), but it is less well understood in these circumstances. This chapter reviews the pathophysiologic factors, clinical management, and prognostic factors in anoxic-ischemic brain injury.


Author(s):  
Ji Y. Chong ◽  
Michael P. Lerario

Hypoxic–ischemic brain injury is common following cardiopulmonary arrest and is associated with high rates of mortality and morbidity. Therapeutic hypothermia has been helpful in increasing survival and functional outcomes in these patients. The neurological examination, neuroimaging studies, and ancillary serological and neurophysiological testing can be helpful in prognostication post-arrest.


2019 ◽  
Vol 10 (1) ◽  
pp. 157-159
Author(s):  
Sung Ho Jang ◽  
Hyeok Gyu Kwon

AbstractThe caudate nucleus, which is vulnerable to hypoxic–ischemic brain injury (HI-BI), is important to cognitive function because it is connected to the prefrontal cortex. Using diffusion tensor tractography (DTT), no study on injury of the prefronto-caudate tract in a patient with HI-BI has been reported so far. Here, we report a patient with severe apathy who showed injury of the prefronto-caudate tract following HI-BI, which was demonstrated by DTT. A 38-year-old female patient suffered HI-BI induced by carbon monoxide poisoning following attempted suicide for a period of approximately four hours. From the onset, the patient showed severe apathy (7 months after onset-the Apathy Scale score was 24 [full score: 42]). Brain MR images taken at seven months after onset showed no abnormality. On 7-month DTT, the neural connectivity of the caudate nucleus to the medial prefrontal cortex (Brodmann area: 10 and 12) and orbitofrontal cortex (Brodmann area: 11 and 13) was decreased in both hemispheres. Using DTT, injury of the prefronto-caudate tract was demonstrated in a patient who showed severe apathy following HI-BI. We believe that injury of the prefronto-caudate tract might be a pathogenetic mechanism of apathy in patients with HI-BI.


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