John Fiske Brown Associates, Inc.

       FORENSIC IMPLICATIONS OF ASPHYXIA

                   By Lori L. Wickham, Ph.D.

If you were to dive into a pool and hold your breath, how long could you spend underwater? Probably less than a minute unless you are David Blaine, an Ama Pearl Diver, or conditioned to lower your metabolic rate like a meditating Yogi.  However, with practice, many people can hold their breath for about two minutes.
What do breath-hold diving, suffocation, strangulation, and drowning have in common?  They all involve progressive asphyxia, concomitant low oxygen [hypoxia], high carbon dioxide [hypercapnia] and acidosis.  The latter is a result of the buildup of lactic acid, a by-product of anaerobic metabolism [without oxygen].  Most of us are familiar with the feeling of pain of lactic acidosis after a demanding workout.  Asphyxia can be limited to a regional tissue deprived of blood [e.g. ischemia] or manifest as blocked respiration in the body as a whole.  

There is a hierarchy within the body in terms of how long different tissues can withstand this deprivation.  In many cases, human extremities can be deprived of blood for more than 30 minutes without damage while the central nervous system, specifically those portions involved in consciousness, will not continue to function for more than a few seconds without oxygen. The disruption of cell metabolism in the tissues and the accumulation of toxic by-products result in patho-physiological consequences such as tissue necrosis, loss of consciousness and death.  Forensic interest may then become a question of causation and how long the asphyxia lasted before death occurred. The latter may be important in cases where family members witnessed the suffering of the decedent.

Lack of oxygen, either partial [hypoxia] or total [anoxia] causes death. Normal room air is approximately 21% oxygen.  Impairment of cognitive and motor function can manifest at oxygen concentrations of 10-15%, loss of consciousness at less than 10%, while death usually occurs at less than 8%.  For example, although hypoxic endurance varies, a person can lose consciousness in 40 seconds and die within a few minutes at ambient oxygen levels as low as  4-6%.

Asphyxial deaths, whether accidental, suicidal or homicidal are grouped by forensic scientists into three generalized categories: Strangulation, Chemical Asphyxia and Suffocation. Most reported murders by asphyxia involve strangulation. An inhaled substance interfering with the body’s ability to use oxygen [e.g. carbon monoxide, butane, and nitrous oxide] characterizes chemical asphyxia. Carbon monoxide blocks the active binding site of hemoglobin [Hb] the protein that carries oxygen in red blood cells. ‘Simple’ asphyxia is another term for oxygen displacement by another gas. When water or another liquid fills the lungs causing asphyxia this is called drowning. There are several variations such as near-drowning, secondary drowning and immersion syndrome. Autoerotic or ‘sexual asphyxia’ by self-strangulation, drowning, choking, and a variety of other means is increasingly reported, especially by the media.

Deaths due to suffocation are often subdivided further, by causation, into those due to entrapment or environmental suffocation, smothering, choking, mechanical asphyxia, mechanical asphyxia combined with smothering and suffocating gases.   Entrapment involves individuals trapped in air-tight enclosures [e.g.  children trapped in abandoned refrigerators].    Environmental suffocation usually involves someone accidentally entering an area depleted of oxygen by a mechanism other than gaseous suffocation.   For example, inhaled fluid displaces air during drowning. Fungal infestations in enclosed areas can also cause lethal oxygen reduction. Smotherings by mechanical obstruction of the nose and mouth are rarely accidental.  However, examples are an alcoholic stupor leading to loss of consciousness and subsequent face compression on pillows or bedclothes and defective cribs with gaps that might impair infant mobility after laying face down.   Criminals also sometimes inadvertently asphyxiate a victim with gags in the mouth or around the face. Choking asphyxia can be homicidal, accidental or even a "natural" result of inflammation of the soft mucosal tissues of the respiratory tract. Some find it surprising that steam inhalation can result in swelling to the point of obstruction in some reactive individuals.  Most reported choking deaths are accidental and involve obstruction of the pharynx and larynx by food.   Accidental inhalation of foreign material is another cause.

When external pressure prevents breathing the term mechanical asphyxia is used. Traumatic asphyxia, positional asphyxia and "riot-crush" deaths are subtypes of mechanical asphyxia.  In traumatic asphyxia, a large mass or heavy weight presses on the victim's chest or upper body preventing breathing.  Survival with minimal or no pathology is surprisingly common even if there is a short loss of consciousness.  More severe cases have included people pinned under a vehicle after a motorway accident or a vehicle falling or rolling onto someone attempting repairs. Traumatic asphyxia has also been reported during police restraint when one or more officers attempt to subdue someone by sitting on their chest. Positional asphyxia is most often an accidental result of someone trapped in a restricted space in a position that prevents breathing. Self-imposed suspended or strapped positions with the head lowered for autoerotic benefits are examples of accidental or suicidal positional asphyxia. Many cases involve alcohol or drug intoxication.    When someone is prevented from breathing or crushed by the bodies of others such as during sports games and rock concerts, the asphyxial death is termed "riot-crush" for obvious reasons. A combination of traumatic asphyxia and smothering can be accidental or homicidal.  The former might involve inadvertently rolling over and incapacitating an infant placed in bed with parents or an older sibling. Burial in a collapsed mine-shaft or cave are other examples. During the early 19^th century, "resurrectionists" Burke and Hare excavated graveyard bodies to sell to medical schools.  They decided preying upon alcoholics would make their job easier.  Burke sat on the victim's chest, used one hand to cover their nose and mouth and the other to close their jaws resulting in traumatic asphyxia and a fresh body - without digging.  This is an example of homicidal traumatic asphyxia in combination with smothering now called "Burking".

During deaths by suffocating gases, ambient oxygen is displaced by another gas.   Common examples are carbon dioxide and methane which are found in mines, sewers and natural gas used for cooking. An interesting case that has received media attention recently involves the mass mortality of people living near volcanoes [www.pbs.org/wgbh/nova/volcanocity]. Lake Nyos and Lake Kivu formed in craters made by dormant volcanoes in Africa. Fissures or springs beneath the craters feed the lakes and deliver high concentrations of carbon dioxide gas which can flow beneath the ambient air to lower elevations thereby decimating entire villages including thousands of people and animals. The locals call these ground hugging plumes of odorless, volcanic carbon dioxide "mazuku" which means "evil wind". Children are often victims because they breathe air nearest to the surface of the earth.

Tolerance to ischemia and asphyxia vary with not only age and special adaptation but also with past medical history and present state of health.  For example, those who have a history of cardiovascular or pulmonary disease may be more susceptible [e.g. heart attack, asthma]. Medications can also affect the body's ability to defend itself against asphyxial threat. 

Postmortem examinations, review of medical records, accident reports and photos taken at the scene are used to analyze and classify asphyxial deaths.  There are non-specific physical signs used to attribute death to asphyxia.  These include visceral congestion via dilation of the venous blood vessels and blood stasis, petechiae, cyanosis and fluidity of the blood.  Petechiae are tiny hemorrhages. Blood vessels, usually small veins, are broken by high intravascular pressure.  They can occur in various parts of the body such as over the surface of the heart and organs, in the eye, the skin and the scalp.  If a large area is affected they may be termed ecchymoses and appear as bruising.    Hemoglobin [Hb] in red blood cells turns from red to blue when it loses oxygen. Veins are described as blue since they carry blood that has released oxygen to the body’s cells, back to the lungs where it can be reoxygenated. As asphyxia progresses and more oxygen is depleted, a dark discoloration of the skin and tissues called cyanosis develops. Cyanotic tissue is described as blue, black or purplish in color depending upon the percentage of deoxygenated blood. After death, changes in blood chemistry and the breakdown of clotting proteins such as fibrin lower the viscosity of the blood; this is sometimes called 'fluidity'. The study of flow is called rheology thus; those who specialize in the study of blood flow behavior are called rheologists or, more specifically, hemorheologists.

As stated earlier, these physical variables are non-specific to asphyxia meaning they can be present after death from other causes.  Furthermore, a case may be complicated by pathology or injuries additional to asphyxia. This information is used by forensic scientists in combination with data on place and manner of death to perform analyses and form opinions. Investigation into asphyxial death often involves a combination of experts who may be clinicians, biomechanical experts and automotive experts who perform accident reconstruction, and chemical or biological scientists.

Further Reading

Beach, H.H. A. and F. Cobb. 1904. Traumatic Asphyxia. Report of a recent case, with a study of the minute pathology, and summary of reported cases. Annals of Surgery 36(4): 481-494.

Feldman, E.A. 1969. Traumatic Asphyxia. The Journal of Trauma, 9(4): 347-353.

Elsner, R. and B. Gooden. 1983. Diving and asphyxia: A comparative study of animals and man. Monographs of the Physiological Society, No. 40. Cambridge University Press, New York, NY, 168 pages.

Elsner, R. and L.L. Wickham. 1988. Implications of physiological studies of seals. Marine Mammal Science, 4(1): 34-43.

Wickham, L.L., R.M. Bauersachs, R.B. Wenby, S. Sowemimo-Coker, H.J. Meiselman, and R. Elsner. 1990. Red cell aggregation and viscoelasticity of blood from seals, swine and man. Biorheology, 27: 191-204.

Hambeck, W. and K. Pueschel. 1981. Death by Railway Accident: Incidence of traumatic asphyxia. The Journal of Trauma, 21(1): 28-51.

Copeland, A. R. 1986. Vehicular-related traumatic asphyxial deaths – Caveat Scrutator. Z. Rechtsmed, 96: 17-22.

DiMaio, V.J. and D. DiMaio. 2001. Asphyxia. In Forensic Pathology, 2^nd Ed., New York, NY, pp. 229-275.

Adams, V.I. and R.S. Vega. 2004. Suffocation in Motor Vehicle Crashes. The American Journal of Forensic Medicine and Pathology, 25(2): 101-107.

Miyashi, S., K. Yoshitome, Y. Yamamoto, T. Naka and H. Ishizu. 2004. Negligent homicide by traumatic asphyxia. International Journal of Legal Medicine, 118: 106-110.

Sauvageau, A. and S. Raclette. 2006. Autoerotic deaths in the literature from 1954 to 2004: A review. Journal of Forensic Science, 51(1): 140-146.