pathophysiology of hanging

 

Suicide by hanging. Atlas of Legal Medicine (Eduard Ritter Von Hoffmann 1989)

Source: National Library of Medicine

 

Despite hanging being a common form of suicide, the precise pathophysiological mechanism(s) involved is (are) poorly understood.

Historically, pathophysiological mechanisms thought to be involved included (Clement et al 2010):

  • respiratory asphyxia,
  • occlusion of blood vessels in the neck causing an interruption of cerebral blood flow, and
  • cardiac inhibition secondary to nerve stimulation.

The Working Group on Human Asphyxiation (WGHA), formed in 2006, has carried out reviews of the literature regarding pathophysiological mechanism theories, the results obtained from animal experiments (and a consideration of their applicability to determining the mechanism of death in humans) and has reviewed filmed suicidal/ accidental hangings in order to describe the sequence of events in such hangings.

A review of data from animal studies (Boghossian et al 2010) - of which the rat is perhaps the best model due to anatomical considerations - revealed (in general):

  • muscular movements ceased after 1-3.5 mins (with early tonic-clonic convulsions being described),
  • complete circulatory collapse occurs between 4-8.5 mins, and
  • cessation of cerebral blood flow, rather than airway obstruction, seems to be the principal cause of respiratory decline.

In a review of filmed hangings (Sauvageau et al 2010), the following general observations were made by the WGHA:

  • rapid loss of consciousness (at 8-18 seconds),
  • convulsions (at 10-19 seconds),
  • decerebrate and decorticate rigidity,
  • loss of muscle tone (between 1 min 38 seconds and 2 mins 15 seconds),
  • isolated body movements 'from time to time' (last between 1 min 2 seconds and 7 mins 31 seconds),
  • deep rhythmic abdominal respiratory movements (last between 1 min 2 seconds and 2 mins 5 seconds).

 

References:

hanging in history - China

 

[The corpse] was suspended from the cross-beam of the north wall within the eastern bedroom of the house facing south, by a hempen rope as thick as one's thumb. The noose was tied round the neck, and knotted at the nape; above it the rope was twice looped around the cross-beam and then tied in a knot, leaving a tail end some two feet long. The top of the head was two feet under the cross-beam, and the feet were suspended two inches above the floor. The head and back touched the wall, and the tongue protruded slightly; below, excreted faeces and urine had soiled both his legs. Upon releasing the rope, the breath issued with a gasp from the mouth and the nose. The rope left a compression bruise mark (around the neck) except for a two inch space at the nape. Elsewhere the body showed no signs of knife-blade wounds or traces of (damage by) wooden (cudgel) or rope. The cross-beam was one span in circumference, three feet long, and projected westwards two feet beyond the edge of an earthen platform (on the ground). From the top of this it was possible (for the deceased) to lead and bring together the rope around the beam.

'Death by hanging' in 'Models for Sealing and Investigating (Feng chen shih)'. Found written on bamboo slips in a tomb at Shui-hu-ti near Yun-meng in Hupei,  China in 1975, and estimated to date between 266 and 246 BC.

'A history of forensic medicine in China', Gwei-Djen L, Needham J, Medical History 1988; 32:357-400

neck dissection in art

 

skinned neck

watercolor, 10.5"x13.5" (dissection revealing musculature of the neck)

 

 

skinned neck 2 (revealing vasculature of the neck)

 

Source: Danny Quirk

Danny says of his work ...

My anatomical works combine classic poses, in dramatic chiaroscuro lighting, with a very contemporary twist… illustrating what’s underneath the skin, and the portrayed figure dissects a region of their body to show the structures that lay beneath.

pressure to the neck and sudden cardiac death

 

Arteries in the neck

Source: Wikipedia

 

The application of pressure to the neck can result in death due to asphyxia, but rare instances have been reported of mild or ‘playful’ pressure being applied to the neck that have resulted in ‘instantaneous death’.

Traditionally these ‘freak accidents’ have been ascribed to ‘vagal inhibition’ or ‘reflex cardiac arrest’, involving stimulation of the carotid sinuses.

The carotid sinus is a dilatation of the lower end of the internal carotid artery, and functions as a baroreceptor (a stretch receptor) responding to changes in vessels induced by the arterial pressure (Standring 2005).

Arterial baroreceptors play a key role in short-term blood pressure control. Impulses arising in the sinus travel up afferent fibres in the carotid sinus nerve (a branch of the glossopharyngeal nerve) and on to the nucleus of the tractus solitarius (NTS) in the medulla.

Stimulation of the NTS inhibits sympathetic nerve impulses to peripheral blood vessels (vasodilatation). Stimulation of the vagal nuclei in the medulla brings about a bradycardia, and the combined effect is to reduce heart rate and reduce blood pressure (Berne and Levy 1996).

 

carotid body anatomy - for full size version see at source

Source: Neuroanatomy at University of British Columbia

 

The baroreflex is very rapid (<1sec), but is inhibited by stimulation of the hypothalamic defence area in ‘fight or flight’ situations. Central pathways controlling the cardiovascular system are complex, involving the cerebral cortex, hypothalamus and cerebellum as well as the medulla (Sunthareswaran 1998).

In addition, alteration in baroreflex sensitivity has been shown to be linked to an increased risk of the development of Ventricular Fibrillation (VF) in experiments on dogs with healed myocardial infarcts (Schawartz et al 1988).

In clinical medicine, it is known that pressure on the carotid sinus can alter the heart rate, and this principle is exploited to elucidate the underlying mechanism and provide prompt treatment of various supraventricular tachycardias as well as differentiate them from ventricular arrhythmias.

 

© WIFM

 

Carotid sinus pressure (© WIFM)

 

Carotid Sinus Pressure (CSP) involves the stimulation of the parasympathetic nervous system resulting in reduced heart rate and reduced cardiac workload. Susceptibility to sympathetic induction of myocardial ischaemia and VF should be reduced, but it is possible that carotid sinus hypersensitivity results in excessive parasympathetic stimulation and cardiac standstill.

This procedure has also been shown to induce atrioventricular (AV) block and asynchrony of ventricular muscle excitability with one case report of VT, providing a substrate for electrical heterogeneity and thus the development of fatal arrhythmias.

It is possible that susceptible individuals have unusually rich ventricular cholinergic innervation, or that following the release of CSP there is a reflex catecholamine release from myocardial stores rather than sympathetic nerve endings, allowing asymmetric distribution and genesis of ventricular ectopics and arrhythmias (Cohen 1972).

Deaths from ‘vagal stimulation’ have been reported for many years (Simpson 1949, Hirsch and Adams 1998), where pressure on the neck, blows to the groin or medical procedures have resulted in the instantaneous death of the victim.

The stimulation of sensory nerves of skin, pharynx, glottis, pleura, peritoneum covering viscera etc result in the afferent stimulation of the parasympathetic nervous system, resulting in a fatal arrhythmia. Vagal stimulation has been found to be profibrillatory to atria, but paradoxically to mitigate ventricular arrhythmias (Willich 1993).

Acute stimulation of the CNS by drugs or electrical stimuli lowers the threshold for cardiac electrical instability, and may evoke a variety of arrhythmias including VF, suggesting a role of the higher centres which has not been fully elucidated.

Critical vasomotor regions of the brain include the 3rd ventricle, the midbrain and medulla oblongata. Interruption of sympathetic and parasympathetic pathways between the brain and heart, for example through trauma, can result in instantaneous death (Hirsch and Adams 1998).

More recently, Purdue (2000) has proposed mechanisms for asphyxial deaths, including mechanisms of sudden death during the application of pressure to the neck.

Novel terms are utilised in an attempt to explain the pathophysiological mechanisms involved, which describe a spectrum of insults leading to cardiac dysfunction;

  • Remotely Stimulated Cardiac Dysfunction (RSCD)
  • Cumulative Cardiac Insult (CCI) and
  • Instantaneous Neurogenic Cardiac Arrest (INCA)

Pressure on the neck during, for example manual strangulation would incorporate elements of neural and humoral mechanisms together with hypoxic changes to bring about CCI and death.

It is suggested that prolonged pressure on the carotid arteries below the level of the carotid sinuses could bring about sympathetic discharge, increasing the risk of ectopic beats and VF (particularly in the setting of fear). Pressure above the level of the sinuses (or on them) would result in parasympathetic discharge and potentially asystole in those with sensitive baroreceptors.

Without the elements of asphyxia and prolonged compression, the concept of INCA is proposed, which represents the extreme end of the CCI spectrum, and involves overwhelming parasympathetic discharge from highly sensitive carotid sinuses.

It is also noted that a similar effect may also be induced by the application of force to other vital ‘nerve centres’ such as the solar plexus (at the pit of the stomach), the front and sides of the neck, the philtrum of the upper lip, the inner aspect of the knees, the cervix and the genitalia (especially the testes).

 

references

 

 

revise your anatomy

 

Revise your anatomy of the neck/ larynx with the help of anatomy resources on the web ..

cervical spine injury

 

patterns of cervical spine injury - for full details, see the excellent Radiology Assistant.

 

Classification of 'hangman's fractures' via Radiology Assistant.

  • Type I (65%)
    • hair-line fracture
    • C2-3 disc normal
  • Type II (28%)
    • displaced C2
    • disrupted C2-3 disc
    • ligamentous rupture with instability
    • C3 anterosuperior compression fracture
  • Type III (7%)
    • displaced C2
    • C2-3 Bilateral interfacet dislocation
    • Severe instability

 

Additional resources on cervical spine trauma evaluation as well as revision resources on cervical spine anatomy, visit this website from the University of Viginia.

Capital punishment - judicial hanging in history

 

Source: Wikimedia Commons

 

 

 

 

 

 

 

 

But see, his face is black and full of blood,

His eye-balls further out than when he lived,

Staring full ghastly like a strangled man;

His hair uprear'd, his nostrils stretched with struggling;

His hands abroad display'd, as one that grasp'd

And tugg'd for life and was by strength subdued:

Look, on the sheets his hair you see, is sticking;

His well-proportion'd beard made rough and rugged,

Like to the summer's corn by tempest lodged.

It cannot be but he was murder'd here;

The least of all these signs were probable.

 

The Earl of Warwick describes the murdered body of Duke Humphrey of Gloucester in Henry VI, part 2 - Act 3, scene 2 by William Shakespeare

 

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