Hello to all!!! I was curious what your experiences were regarding treatment of cardiac arrest victims secondary to hanging. Do you treat as a traumatic or medical arrest (or some hybrid tx)? Of course c-spine immobilization goes without saying, but beyond that. Intubate or not? Cold saline or not? Topic came up recently. I've tried researching online and have had trouble finding good data regarding most common cause of cardiac arrest in hanging victims (spinal fracture, asphyxia, vasculature being cutoff, etc.). Looking forward to any information this wonderful community can provide. Any links to research/data showing most common cause of arrest in these circumstances would be appreciated. I guess my "googling" skills are not as good as I thought they were.
Hm, don't see too many hanging victims that I'd bother working, mostly I've heard of people getting to them just in time, or way too late.
Most victims are asphyxic (and if they do it right, a nice drop breaking cervical vertebrae will result in secondary aspyxia), but if you get to the point where asphyxia causes cardiac arrest it's probably too late. Otherwise, I'd treat as a medical arrest. I'm not even certain C-spine precautions are necessary in all situations, if you can prove they didn't fall very far (pretty unlikely but theoretically possible).
I admitted four kids to the Pediatric Intensive Care Unit who attempted suicide by hanging. There was little, if any, published experience on managing survivors as almost all the articles came from the pathology literature and autopsies. Those who had brain function, as I recall, showed signs of basilar brain injury you would expect from congestion of the jugular vein and back-up of blood in that drainage area with subsequent damage. The jugular vein is more easily occluded than the carotid artery or trachea. As you read through the following abstracts you see that even judicial hangings, set up for a fall to produce sufficient force to fracture vertebrae, may not break the neck. They may separate the brain stem from the spinal cord.
Of note, the cardiac output in the non-survivors did not increase despite fluid administration or inotropic drugs.
Med Sci Law. 2009 Jan;49(1):18-26.
Cause of death in judicial hanging: a review and case study.
The cause of death in judicial hanging is controversial and often attributed to 'hangman's fracture' of the second cervical vertebra. Research has shown that such fractures are the exception in judicial hangings and the cause of death can be attributed to a range of head and neck injuries, particularly compression or rupture of the vertebral and carotid arteries leading to cerebral ischaemia. The rapidity of loss of consciousness and death is highly dependent upon knot positioning and the length of drop which has varied through the history of hanging as a capital punishment in the UK. The skeletal remains of Mr. George Kelly, wrongfully hanged for murder at Walton prison, Liverpool (1950) were exhumed, examined and are reported on herein. The first cervical vertebra was found to be fractured but no 'hangman's fracture' of the axis--second cervical vertebra--was present. The hangman (Mr. Albert Pierrepoint) has been quoted as stating that the hanging of Mr Kelly took longer than 'it should have' (Dernley and Newman, 1989) but no skeletal evidence of death by strangulation was found by the authors. Unconsciousness, if not death, would probably have been rapid due to vertebral artery damage as a result of the observed neck fracture, although this cannot be concluded with absolute certainty.
J Forensic Sci. 2010 Sep;55(5):1268-71.
Mechanism of death in hanging: a historical review of the evolution of pathophysiological hypotheses.
In cases of hanging, the exact mechanism leading to death has yet to be elucidated. Most of our contemporary knowledge is still based on writings from the end of the 19th and the beginning of the 20th century. This article reviews the historic experiments that shaped our current theories. Medico-legal textbooks written in English and French from 1870 to 1930 were reviewed. Various animals, such as rabbits, mice, and dogs, have been used to develop animal models of hanging. Limited human studies on cadavers and judicial hangings have provided some additional insight into the pathophysiology of death by hanging. The main pathophysiological theories described were respiratory asphyxia, interruption to cerebral blood flow because of occlusion of vessels in the neck, and cardiac inhibition secondary to nerve stimulation.
J Forensic Sci. 2010 Sep;55(5):1272-7.
Respiratory, circulatory, and neurological responses to hanging: a review of animal models.
The pathophysiology of hanging is still poorly understood. This article presents a review of eight animal models: four models of isolated occlusion of the vessels of the neck (group 1), one model of combined tracheal and vessel occlusion (group 2), and three models of true animal hanging (group 3). Occlusion of the airway passages in group 2 did not accelerate respiratory arrest compared to group 1. Cessation of cerebral blood flow, rather than airway obstruction, seems to be the main cause of respiratory decline. In general, muscular movements ceased after 1-3.5 min and early generalized tonic-clonic convulsions were described. Complete circulatory collapse seems to occur between 4 and 8.5 min.
Pediatr Neurol. 1991 Sep-Oct;7(5):369-74.
CBF and CBF/PCO2 reactivity in childhood strangulation.
Four children with self-inflicted strangulation injuries had cerebral blood flow determined by stable xenon computed tomography (XeCTCBF) within 24 hours of admission. All had suffered a severe hypoxic-ischemic cerebral injury; 3 initially had fixed pupils, all were apneic with varying bradyarrhythmias, and the initial mean arterial pH was 7.26 (+/- 0.18). The initial blood glucose values were greater than 300 mg/dl (334 and 351 mg/dl) in the 2 patients who died compared to the 2 who survived (104 and 295 mg/dl). The cardiac index was depressed during the first several days of hospitalization in the 2 patients who died (less than 2.0 L/min/m2) compared to the 2 who survived. Total CBF was normal (63 +/- 8 ml/min/100 gm) and local variations in CBF were present. PCO2 reactivity was determined by hyperventilating the 4 patients for 20 min from an end tidal PCO2 of 39 +/- 3 torr to 29 +/- 1 torr and then repeating the XeCTCBF study. Marked regional variability in the CBF/PCO2 response was observed, ranging from 0.5-5.5 ml/min/100 gm/torr PCO2. In the 2 patients who died, the CBF/PCO2 was decreased (1.2 ml/min/100 gm/torr PCO2) compared to the 2 patients who survived (2.1 ml/min/100 gm/torr PCO2). Although CBF was normal in these 4 children, the hyperventilation response was depressed, variable, and even paradoxical which may be important in the evolution of further brain injury and is a critical factor in deciding whether hyperventilation may be of clinical benefit.
In my area a hanging victim without a pulse is considered a traumatic arrest. In this area a traumatic arrest (of any kind) is not worked once lack of pulse or a non shockable rhythm is noted. They are DRT and the scene is handed over to PD.
Assuming a pulse exists at time of EMS contact the patient is considered a priority trauma patient.
Loss of pulse during a trauma transport results in a call to Med control who 99 times out of 100 will then request resuscitation efforts halted.