mechanisms of death
And when i'm a man - Wayne Chisnall 1998
A conceptual difficulty when learning about the forensic pathology of trauma, and sudden or unexpected death, is 'why did the individual die when they did?'.
Medical students - and pathology trainees - are taught what the relevant signs, symptoms and pathological findings are in diseases and conditions, but rarely are they taught about the pathophysiological disturbances that accompany potentially fatal diseases/ conditions. When dealing with traumatic events, such pathophysiological disturbances are also neglected, in favour of identifying the anatomic/ pathologic abnormality that can be seen - either by the 'naked eye' or under the microscope.
The most comprehensive resource for reviewing such 'mechanisms of death' can be found in 'Spitz and Fisher's Medicolegal Investigation of Death', and the following notes are adapted from this source.
The principle mechanisms of interest are those having an adverse effect on the heart, the brain, or both.
[Adams VI, Flomenbaum MA, Hirsch CS. Mechanisms of death. Chapter 9 In: Spitz and Fisher's Medicolegal Investigation of Death, 4th Edition (2006), Spitz WU (Ed), Charles C Thomas, Springfield, Illinois, USA]
electrical disturbances of heart and central nervous system
- electrical irritability
- electrical depression
exogenous electrical disturbances
Electric chair - Andy Warhol
Source: Mindy Nierenberg
- Alternating Current (AC) passing through the heart during the vulnerable repolarisation phase can precipitate Ventricular Fibrillation (VF)
- AC/ Direct Current (DC) can provoke tetany if the current is high enough
- Return of sinus rhythm is possible following removal of DC source
- The effect of 'electrocution' on the brain is poorly described in the literature
Electrocution (from 30 ways to die of electrocution)
conversion of impact mechanical energy to electrical energy
A proportion of impact (mechanical) kinetic energy is converted in the body to electrical energy.
- in the heart, conversion of impact mechanical energy - from a blow to the precordium - can lead to 'cardiac concussion' ('commotio cordis'), and result in VF or asystole
- in the central nervous system, transmission of mechanical energy can lead to respiratory paralysis or autonomic-medicated asystole
non-impact pressure gradients in vital areas
- Subarachnoid haemorrhage (SAH) can lead to:
- brainstem/ hypothalamic tamponade leading to autonomic-mediated ventricular arrhythmias;
- cerebral blood vessel vasospasm leading to autonomic-mediated arrhythmias;
- brainstem tamponade leading to respiratory arrest
- Cerebral herniation can cause failure of medularry respiratory centres and loss of vasomotor centre abnormalities
- Compression of the heart by a pericardial fluid accumulation (cardiac tamponade as a consequence of, for example, a rapidly accumulating haemopericardium) interferes with cardiac chamber filling and reduces cardiac output. Central blood flow decreases and the heart becomes hypoxic, leading to bradycardia and PEA.
exogenous chemical interference with electrochemical cellular communication
- CNS excitation (leading to seizures) - e.g. cocaine, theophylline, isoniazid
- CNS depression (leading to 'reduced level of consciousness', 'failure to protect the airways', 'aspiration pneumonitis/ pneumonia' etc) - e.g. heroin/ morphine, alcohol
- CNS depression with or without cardiac arrhythmia - e.g. cocaine, anti-arrhythmics, tricyclic antidepressants, phenothiazines
- Direct cardiac 'irritant' - e.g. alcohol
- interference with neuromuscular/ synaptic signal transmission - e.g. curare-induced hypoxia due to diaphragmatic paralysis
thermal physiological disturbance
- elevated temperature (hyperthermia)
- reduced temperature (hypothermia) - depressed cardiac conduction, ectopic beats and VF
microscopy in multiple organ failure following hyperthermia
'Hyperacute heart muscle cell injury' (contraction band necrosis/ myofibril degeneration)
Renal tubular casts in a setting of acute renal failure
Extensive liver necrosis
(H&E staining - low power)
(H&E staining - higher power)
obstruction or diversion of central blood circulation
- diversion of blood volume
- exsanguination (in general, rapid loss of 1/3rd of the blood volume results in shock whilst rapid loss of 1/2 is fatal due to inability to perfuse the coronary circulation)
- acute neurogenic shock (disordered agonal autonomic function results in a redistribution of circulating blood volume to the musculoskeletal system, e.g. following concussive blunt force head injury or an injury between the IIIrd ventricle in the brain and the mid-cervical spinal cord)
- anaphylactic shock (fluid shifts from plasma to the extracellular compartment following histamine release due to mast cell activation and degranulation)
- obstruction of blood volume (inadequate supply of blood to the lungs to be oxygenated leads to cardiac hypoxia, bradycardia and asystole)
anaphylaxis - one minute med school tutorial
obstruction of arterial blood supply to the heart or CNS
- to the heart (leading to coronary insufficiency, regional cardiac ischaemia and arrhythmias):
- to the brain (leading to 'stroke' or brainstem ischaemia and sudden death) - similar causes to those above in the heart/ coronary circulation
- external compression of blood vessels in the neck
Arteries in the neck
Source: Gray's Anatomy via Wikipedia
mechanical interference with respiration
- pressure to the neck - tongue pushed into the oropharynx occluding the upper airways
- occlusion of the mouth/ nose ('suffocation')
- obstruction of upper airways due to the position of the head on the neck (i.e. bent forwards) in a setting of intoxication, concussion or neurological disease ('positional asphyxiation')
- compression of the chest preventing adequate ventilation movements (e.g. 'traumatic asphyxiation', 'pressing')
- occlusion of the airways from within e.g. by food or foreign bodies in intoxicated - or otherwise neurologically compromised - individuals
- pneumothorax leading to pulmonary vascular 'shunts' and hypoxaemia
- 'flail chest' following blunt force chest trauma, causing paradoxical inward chest movements on inspiration and leading to hypoxaemia
- chemical aspiration pneumonitis leading to hypoxaemia/ intra-pulmonary 'shunts'
chemical interference with oxygen metabolism
- as a consequence of a reduced level of oxygen in the inspired air mixture
- in confined spaces (e.g. caves and storage tanks etc)
- reduced oxygen partial pressures following oxygen displacement from the confined space by carbon dioxide or gaseous products, for example
- as a consequence of breathing in an oxygen poor medium e.g. drowning
- breathing in carbon monoxide (irreversibly binds to haemoglobin) or cyanide (poisons the mitochondrial cytochromes)
Wrinkling of the skin of the hand following recovery of body from water (Johann Ludwig Caspar 1864)
Source: National Library of Medicine
- Inadequate tissue perfusion manifested by arterial hypotension as a consequence of:
public safety campaign animation 'Dumb ways to die' (Metro Trains Melbourne 2012)
deaths involving complex pathophysiological interactions - deaths in custody and 'struggle against restraint'
Taser conducted electrical weapons
Pathophysiology of death
|By||Dr Richard Jones|
Pathophysiology of death
A difficult concept to grasp in forensic pathology is 'Why did that person die now?', which involves a consideration of the pathophysiology of trauma, natural disease, and death.
How well are these issues covered in your medical training?
How could they be incorporated into the undergraduate medical curriculum?
Let me know your thoughts.