L’expert, l’expertise médicale et la contre-expertise.


par K. B.

Source: http://www.lequotidien-oran.com/index.php?news=5163628

L’Algérie accorde un intérêt croissant à la criminologie et à la médecine légale, compte tenu des mutations que connaît la société algérienne, a souligné le Pr A. Oussadit, chef de service de la médecine légale au CHU de Tlemcen.

Dans une déclaration à notre journal, en marge des deuxièmes Rencontres régionales de médecine légale qui s’est tenu le 26 janvier 2012 à l’auditorium de la faculté de médecine Chahid Acimi à Tlemcen sous le thème «L’expert, l’expertise médicale et la contre-expertise», le Pr A. Oussadit a estimé que le médecin se livrant à la pratique de l’expertise est susceptible d’engager sa responsabilité, qu’il s’agisse d’un médecin expert judiciaire mandaté par l’autorité judiciaire pénale civile ou administrative, ou d’un conseil désigné par une compagnie d’assurance ou par un particulier. Il a dans ce contexte souligné que le médecin expert est un auxiliaire de justice, car le magistrat a besoin de son avis technique. Sa mission est de reprendre tous les chefs de préjudice, de définir tout ce qui a changé par rapport à l’état de la personne antérieur à l’accident, afin que celle-ci soit indemnisée. Le médecin expert ne peut répondre à autre chose qu’aux questions qui lui sont posées dans le cadre de sa mission : il ne peut pas faire état d’éléments étrangers à sa mission. Il convoque les parties et les entend, puis il fait un rapport.

Le Pr Oussadit a rappelé aussi la différence qui existe entre le médecin expert et le médecin conseil. «Le médecin expert est inscrit sur la liste des experts ; il ne dépend que du tribunal et est indépendant des parties. Le médecin conseil travaille pour les compagnies d’assurances ou pour la victime». L’importance de cette rencontre pluridisciplinaire regroupant les praticiens du droit et de la médecine réside, tient à préciser le Pr Oussadit, dans le partage du savoir entre les participants, d’autant plus que les thèmes au programme portent, entre autres, sur l’aléa thérapeutique chez l’homme.

D’autres exposés furent donnés. Le Pr Meguenni Kamel (faculté de médecine de Tlemcen) : l’importance de l’expertise en matière de preuve pénale ; M. Guedidène Ismaïl, procureur de la République adjoint près le tribunal de Tlemcen : expertise en matière de responsabilité médicale ; le Pr Boublenza Abdellatif (faculté de médecine de Sidi Bel-Abbès) : responsabilité du médecin expert ; le Pr Aboubekr Abdelmadjid (faculté de médecine d’Oran) : responsabilité des médecins experts ; le Pr Belhadj Lahcen (faculté de médecine Sidi Bel-Abbès).

A noter qu’un hommage particulier a été rendu au cours de ces deuxièmes journées de médecine légale au regretté Professeur Mourad Hannouz, décédé il y a dix ans. Ses amis et ses élèves se sont réunis à 9 heures à la faculté de médecine de Tlemcen pour témoigner de son parcours et de son enseignement et honorer sa mémoire et son souvenir. Le professeur Hannouz est natif de Constantine, le 5 juillet 1933. Docteur en médecine, il milita activement à l’UGEMA et participa à la grève de 1956 décidée par le FLN. A l’indépendance, il rejoint les rangs de l’ANP à Sidi Bel Abbès avec le grade de lieutenant. En 1965, il s’installe à Saïda et assume la fonction de directeur départemental de la santé (DDS). Au début des années soixante-dix, il débute des études spécialisées en France et obtient quatre diplômes en médecine légale, droit médical, réparation juridique du dommage corporel et criminologie. En 1976, il s’installe à Oran et crée le premier service de médecine légale de l’Ouest. Il soutient brillamment une thèse de doctorat d’Etat en sciences médicales. Il a présenté la Société algérienne de médecine légale et a été membre du conseil d’administration de la Société méditerranéenne de médecine légale. Il a publié de nombreux manuels de droit médical et de règlementation.

  • Source: http://www.lequotidien-oran.com/index.php?news=5163628

Asphyxial Deaths and Petechiae: A Review


Susan F. Ely,1M.D., M.P.H. and Charles S. Hirsch,1M.D.

REFERENCE: Ely SF, Hirsch CS. Asphyxial deaths and pe-techiae: a review. J Forensic Sci 2000;45(6):1274–1277.

ABSTRACT: Conjunctival and facial petechiae, although nonspe-cific findings, are considered hallmarks of asphyxial deaths. Con­sensus in the literature suggests that their pathogenesis is related to the combined effects of increased cephalic venous pressure and hy-poxic damage to endothelial cells. Despite the common knowledge that they are neither predictable findings in all asphyxial deaths nor rare in natural, nonaphyxial deaths, the belief persists that petechiae are corroborative evidence of asphyxia. We suggest that a clear, physiologically based understanding of the pathogenesis of pe-techiae of the head is critical for their appropriate interpretation. We present a review of the literature and the basis of our conclusion that conjunctival and facial petechiae are the product of purely mechan-ical vascular phenomena, unrelated to asphyxia or hypoxia.

KEYWORDS: forensic science, petechiae, asphyxia, conjunctival petechiae, facial petechiae

Conjunctival and facial petechiae have been regarded as classic signs of asphyxial deaths (1–11). First described by Tardieu in the nineteenth century, external and visceral petechiae have since been interpreted as hypoxia-related sequelae of asphyxia, sometimes be-ing attributed in part to “mechanical obstruction of the upper air-way” (12,13). Despite consensus in the literature that cephalic pe-techiae are not found in all asphyxial deaths, and that they are observed commonly in natural deaths without an asphyxial mech-anism (2–7,13–15), the view that petechiae and asphyxia are causally linked continues to be perpetuated, without regard to the inherent inconsistencies central to that theory. Potential confusion generated by the foregoing misconception bears out most precari-ously in courts of law, where forensically and scientifically sound pathogenetic conclusions are critical for the proper adjudication of criminal proceedings. In that setting, the presence of conjunctival and facial petechiae traditionally has been used as compelling evi­dence in support of an asphyxial death, while their absence has cast serious doubt on that possibility. We suggest that a clear under-standing of the pathogenesis of petechiae of the head increases the likelihood of their appropriate interpretation.

Many authors have described the incidence of conjunctival pe-techiae in nonasphyxial and asphyxial deaths, but there is a dearth of literature comprehensively addressing their pathogenesis. Fur-thermore, much of the literature on petechiae cannot be compared and contrasted because studies report petechiae as either present or absent, one being as good as a million. Such an either/or criterion disregards the reality of common experience and equates a single,

1Office of Chief Medical Examiner of the City of New York, New York Uni-versity School of Medicine, Department of Forensic Medicine, New York, NY.

Received 11 Oct. 1999; and in revised form 10 Dec. 1999; accepted 21 Dec. 1999.

subtle conjunctival red dot with showers of conjunctival and facial petechiae too numerous to count. Granted, in rare instances, an iso-lated petechia may be an important finding in the context of a com­plete case study, but to base our understanding of an entire subject on three standard deviation outliers is the equivalent of a tiny tail wagging a large dog. Therefore, this paper describes the pathogen-esis of conjunctival and facial petechiae on the basis of mechanical phenomena in order to clarify inconsistencies and vagaries in the literature. First we present a review of the literature and then our conclusions regarding petechiae of the head as they pertain to as-phyxial and nonasphyxial deaths. We will not address the patho-genesis of visceral petechiae in our review.

Definition

Asphyxia is broadly defined as the interference with the intake or utilization of oxygen, combined with the failure to eliminate carbon dioxide (6). Although all end organs are ultimately affected by asphyxia, the brain is most sensitive to it effects. The array of circumstances leading to asphyxial deaths varies widely. Together, they present some of the more vexing challenges in medicolegal death investigation and include such disparate mechanisms as cer­vical vascular obstruction, lower airway obstruction, smothering, chest compression, suffocation by asphyxiant gases, entrapment, and drowning.

Literature Review

Tardieu was the first to describe minute hemorrhages due to rup­ture of small blood vessels on the surfaces of the lungs, heart, and other body parts, and regarded them as “characteristic of death from suffocation” (12). The discussion within the forensic commu-nity that followed (10,16–21) became the forerunner of the contro-versy and confusion that remains today, including that surrounding the pathogenesis of the thoracic visceral petechiae sometimes ob-served in Sudden Infant Death Syndrome (SIDS). There does exist, however, wide agreement today that what are now known as “Tardieu spots” are the result of intense lividity, leading to post-mortem rupture of dependently engorged blood vessels, entirely unrelated to asphyxia or any other mechanism of death. The occa-sional reference still made to them in the literature as antemortem petechiae or “asphyxial signs” betrays a misconception of their cur-rent meaning (6–7,10,21).

Luke was the first to propose that increased intracranial vascular pressure is the basis for the development of petechiae of the head in deaths involving compression of the neck or chest. In his 1967 review of strangulations in New York City, he reported that exter-nal petechiae, found in approximately 50% of the cases reviewed, were more prevalent on the conjunctivae than the face, slightly more prominent on the face than on the scalp, and seemed to be en-hanced by the use of a ligature (14). He later theorized that the in-

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ELY AND HIRSCH • ASPHYXIA AND PETECHIAE 1275

creased prevalence of petechiae in ligature strangulations was due to the probability that “disproportionate venous/arterial compro­mise may be more effectively accomplished” with a ligature than with the hands alone (15). He explained that these petechiae oc-curred as a result of impairment of intracranial venous egress while arterial flow to the head continued, a “practically universal” phe-nomenon in ligature strangulations, partial suspension hangings, and thoracic compressions (1). Despite his seeming understanding, however, he went on to say that the pathogenesis of petechiae in these deaths had yet to be fully elucidated. In 1985, Luke and his colleagues elaborated on this theme in a retrospective study of hanging deaths (15). They concluded that the small vessel and in-tracapillary pressures in the head leading to the formation of pe-techiae of the conjunctivae and face should reflect the extent of carotid and vertebral artery occlusion, and that this, in turn, was de­pendent upon the amount of compressive ligature pressure pro-duced by the degree of body suspension. The effects of the consis-tency and size of the ligature were not specifically addressed. Other authors have supported this contention, but have further suggested that the petechiae result from elevated venous pressure combined with hypoxic injury to endothelial cells caused by venous stasis and tissue acidosis (2,4,5,9,10,13,16,18,22).

Rao and Wetli were the first to apply the mechanical theory of the formation of conjunctival petechiae to nonasphyxial deaths in which there is increased cephalic venous pressure without neck or chest compression, per se (13). They included sudden cardiovascu-lar deaths, particularly those with acute right heart failure, and in­stances in which individuals die with their faces prone as examples. They found, in fact, in their review of 5000 autopsy reports over nearly a two-year period, that conjuctival petechiae were observed most frequently in deaths due to natural causes. Their study con-tained no information or description of the number of petechiae ob-served in “positive” instances. When seen in asphyxial deaths, however, specifically, “homicidal asphyxiation” and mechanical chest compression (traumatic asphyxia), they agreed with other au-thors’ contentions that the petechiae resulted from a combination of hypoxia and increased cephalic vascular pressure. This theory was further applied to nonasphyxial deaths in a study by Hood et al. that described the presence of conjunctival petechiae in individuals who had undergone attempted cardiopulmonary resuscitation prior to death (2). All decedents had petechiae of the conjunctivae, eye-lids, and/or cheeks that were felt to be caused by perimortal resus-citative efforts, and unrelated to the mechanisms of death. Interest-ingly, the causes of death that were thought to be unrelated to the development of the petechiae in these decedents included atherosclerotic cardiovascular disease with an acute myocardial in-farct, epilepsy, and gunshot wounds to the head, all known occa-sionally to be associated with conjunctival petechiae (5,13). The authors concluded that petechiae of the head occurred when re-peated forceful resuscitative chest compressions caused increased pressure in small blood vessels that had been damaged as a result of hypoxia in a dying individual, leading to vascular rupture and blood extravasation into the surrounding tissues. They went on to say that hypoxia alone, without increased vascular pressure, was insufficient to produce such petechiae. They suggested that the combined amount of hypoxia and pressure needed to produce con-junctival petechiae was “not great,” even in the living subject. They based this contention on a study in which healthy volunteers were placed in a head-down, vertical position as a means of determining the ocular manifestations of gravity inversion (23). After only one minute of inversion, the resultant ocular findings included orbital congestion, conjunctival hyperemia, and petechiae of the conjunc-

tivae and upper eyelids. However, no subject lost consciousness during testing. Moreover, intraocular pressures were found to reach 80% of their maximal level within ten to fifteen seconds of inver­sion, and no statement was made suggesting that vascular hypoxic damage was contributory to the development of the petechiae. The forensic literature mentions some of these same physical findings in descriptions of fatalities due to positional asphyxia in victims of accidental, head-down “reverse suspension,” but without specific discussions of the pathogenesis of cephalic congestion or petechiae of the head (24,25).

Other scenarios have been described as mechanical causes of conjunctival and facial petechiae in living patients and in victims of natural, nonasphyxial deaths, including status epilepticus, labor and delivery, and severe or sustained episodes of vomiting, cough-ing, sneezing, or respiratory stridor, as seen in bronchial asthma or croup (5,13,26,27). The underlying pathophysiologic mechanism suggested in these settings is the prolonged and/or forceful abdom­inal and thoracic muscular contractions resulting in reflux of blood from the right heart, which causes increased pressure in the valve-less veins of the head and neck. The mechanical contribution of a concurrently closed glottis in association with thoracoabdominal compression (the Valsalva maneuver) in the production of in-creased cephalic venous pressures also is mentioned in the litera-ture describing the facial plethora and petechiae accompanying prolonged chest compression in instances of traumatic asphyxia (26,28). The authors of these papers suggest that the glottis closes as part of a “pre-impact fear response” or panic.

The characteristic distribution of petechiae in cases of chest or neck compression has been addressed infrequently in the derma-tology and forensic literature (7,26). In a case report describing the pathophysiologic features of traumatic asphyxia, Lowe et al. theo-rized that is was the lack of tissue support around conjunctival cap-illaries that accounted for the predictable subconjunctival hemor-rhage, a nearly constant feature of traumatic asphyxia.

Asphyxial deaths in which facial and conjunctival petechiae are distinctly uncommon include those due to smothering (facial wedgings, those involving plastic bags or gags, and all forms of homicidal smothering), overlaying of children, choking, suffocat-ing gases, entrapment, and drowning (5,6). Interestingly, however, at least one author has noted the occasional finding of very fine fa-cial/conjunctival petechiae in deaths that involve the gagging or homicidal smothering of elderly individuals; an explanation for this observation, however, was not offered (5). Moreover, in those few deaths due to plastic bag suffocation in which conjunctival pe-techiae have been observed, neck ligatures usually were used to se-cure the bag in place; in those deaths without petechiae, no such ligatures were used (22,29). In accidental autoerotic deaths, the presence of petechiae correlates with the mechanism of asphyxia; specifically, in incomplete suspension hangings and ligature stran­gulations, petechiae more commonly are found, whereas, in deaths involving plastic bags or gags, they are not.

The presence or absence of petechiae is not specifically ad-dressed in textbook discussions of deaths due to carotid sleeper and bar arm control/choke holds. Suggested mechanisms of these deaths include anoxia, particularly with the airway obstruction of bar arm holds, carotid sinus massage leading to an arrhythmia, a catechol surge due to “air hunger,” and carotid and/or jugular vas-cular occlusion (5). Reay and Eisele found conjunctival petechiae, more prominently on the left side, in two cases of carotid sleeper hold deaths that occured during law enforcement activities (30). In each case, the hold was used for an unspecified “brief” period, dur-ing which time an intense struggle took place. An explanation for

1276 JOURNAL OF FORENSIC SCIENCES

the development of petechiae in this setting, however, was not offered.

Discussion

Excluding those related to infectious, coagulopathic, or mi-croembolic etiologies, we conclude that petechiae of the head are the product of purely mechanical vascular phenomena: namely, im-paired or obstructed venous return in the presence of continued ar-terial input. As pressure builds in venules and capillaries, particu-larly those with little surrounding connective tissue support, such as the conjunctivae and eyelids, vascular rupture produces pe-techiae. The likelihood of this occurrence is directly proportional to the degree of venous obstruction and inversely proportional to that of arterial compression at or above the level of the heart. Nearly 4.5 lb (2 kg) of pressure is required to compress the jugular veins, whereas 11 and 66 lb (5 and 30 kg) are required to compress the carotid and vertebral arteries, respectively (15,31); therefore, an in-termediate amount of force simultaneously applied to both results in venous compression before arterial (2,6,15). This is similarly ap­plicable to the right and left sides of the heart. If the compressive pressure to the chest or neck is great enough to obstruct venous re-turn from the head, but not enough to obstruct arterial flow to it, cephalic venous pressure will rise, as will the probability of small vessel rupture. A violent struggle that increases cardiac output and raises blood pressure therefore enhances the occurrence of pe-techiae. Alternatively, if the applied force is sufficiently great to obstruct arterial flow, venous engorgement and rupture will not oc-cur. An analogous mechanism resulting in elevated cephalic ve-nous pressure without compression occurs with a precipitous im-pairment of venous return to the heart, such as that seen in acute right heart failure.

A clinical illustration of this vascular pressure phenomenon has been demonstrated elegantly with the capillary fragility test, or tourniquet test. Although now replaced by laboratory diagnostics, the tourniquet test was used years ago to assess vascular integrity by maintaining sphingomanometric pressure between that of sys-tolic and diastolic for a duration of 5 min on an upper extremity. The number of petechiae observed within a 3 cm diameter distal to the tourniquet served as an indicator of mechanical vascular in-tegrity; the presence of less than five petechiae was considered nor­mal. Since arterial perfusion continued during testing, the pe-techiae were correctly interpreted as products of vascular rupture due to obstructed venous egress, rather than hypoxia (32).

Most authors agree that increased venous pressure is requisite in the development of conjunctival and facial petechiae, irrespective of whether the death is due to an asphyxial or natural, nonasphyx-ial cause. This conclusion is supported by the fact that petechiae characteristically and predictably are present in deaths that are pre-ceded by impairment of venous egress from the head, while con-tinuous or intermittent arterial perfusion to it continues. Examples of such deaths include those involving partial suspension hanging, ligature or manual strangulation, traumatic asphyxia/chest crush-ing injury, plastic bag-ligature suffocation, carotid sleeper holds with a concomitant struggle, acute right heart failure, status epilep-ticus, and those deaths preceded by a vigorous cardiopulmonary re-suscitative effort, or prolonged or violent paroxysms of coughing or vomiting. Equally supportive of the vascular pressure mecha-nism is the fact that asphyxial deaths either with no impairment of venous return from the head or with arterial obstruction at or above the level of the heart characteristically lack facial and conjunctival petechiae (e.g., full suspension hanging, plastic bag suffocation,

laryngotracheal obstruction, including bar arm holds and choking, asphyxiation by suffocating gases, smothering, overlay deaths in children, entrapment, and drowning).

Considering all of the foregoing observations, it is our con­tention that no relationship exists between the development of pe-techiae and the presence or absence of asphyxia. Rather, it is ve-nous congestion without arterial obstruction that pathogenetically links the development of petechiae in these deaths, otherwise often disparate in their causes, mechanisms, and manners. Typically, the more intense the facial plethora, the more florid the petechial erup­tion. A possible explanation for the occasional observation of con-junctival petechiae in homicidal smotherings of elderly victims is the increased cephalic venous pressure of the Valsalva effect caused by struggling and screaming against an obstructed upper airway. This, together with increased cardiac output, elevated blood pressure, and the fragile vasculature and inelastic surround-ing connective tissue of elderly persons, may lead to facial and con-junctival microvascular rupture. Conversely, the occasional ab­sence of facial plethora and petechiae in victims of chest compression (traumatic asphyxia) is best explained by an over-whelming crushing force that effectively compresess the left ven-tricle and arrests further cardiac output, thereby precluding cephalic venous congestion.

Further support for a purely mechanical basis for the develop­ment of petechiae lies in the fact that, when observed on the head, they are more likely to be found on the conjunctivae and eyelids (7,9,14,17,22,26,28). Luke found, in fact, in his 1985 review of hanging deaths, that although conjunctival petechiae were com-monly observed as isolated findings, petechiae of the facial skin were never seen without those of the conjunctivae (15). This distri­bution is best explained by the relative lack of support and resis­tance offered by the surrounding tissues in and around the con-junctival and palpebral capillaries. As pressure mounts in the microvasculature, the likelihood of rupture is inversely correlated with the tenacity of the surrounding connective tissue and its abil-ity to prevent and/or tamponade blood extravasation. Surely, the capillary endothelium of the conjunctivae and eyelids is no more susceptible to the effects of hypoxia and tissue acidosis than is the capillary endothelium of the thick skin of the face. Yet, petechiae are distinctly more prevalent in the conjunctivae and eyelids.

The literature suggests that it is the combined effects of in-creased vascular pressure and hypoxic microvasculature that lead to petechiae of the head. Although this is difficult to disprove, the addition of hypoxia to the pathogenetic equation is unnecessary and misleading. Without invoking venous stasis and hypoxia-re-lated increased vascular permeability, the pathogenesis of conjunc-tival and facial petechiae is sufficiently explained by vascular pres­sure increases and microanatomy alone; all available data support this mechanism. Moreover, conjunctival petechiae have been ob-served in surviving victims of attempted strangulation, suggesting cephalic venous congestion, rather than life-threatening asphyxia, as the mechanism of microvascular rupture. A study examining both living and dead victims of strangulation reported conjunctival petechiae in 14 out of 79 surviving victims, only half of whom had suffered sufficient oxygen deprivation to lose consciousness during the assault (33). Some of these surviving victims actually had a more florid and pronounced petechial eruption than that of their de-ceased counterparts. Despite these data, the speculation that hy-poxia must play a role has generated the erroneous conclusion that petechiae and asphyxia are causally related. The perpetuation of this belief betrays an attachment to dogma that has no basis in sci­ence or logic. Some authors have actually suggested an instanta-

ELY AND HIRSCH • ASPHYXIA AND PETECHIAE 1277

neous neural mechanism of death (as opposed to complete arterial obstruction) in pale-faced victims of full suspension hangings, as a means of explaining the absence of the expected “asphyxia-in-duced” petechiae in those cases (8).

We conclude that hypoxia is unrelated to the pathogenesis of pe-techiae in deaths due to compression of the neck or chest. Facial and conjunctival petechiae develop in a variety of circumstances in which cephalic plethora, not asphyxia, is the final common path-way. We know of no evidence whatever to support the contention that hypoxia of a duration up to a few minutes, i.e., sufficient to be lethal, produces capillary fragility or any hemorrhage-inducing al­teration of the physical properties of capillary endothelium in the conjunctivae or any other location. In fact, compelling evidence ex-ists to the contrary. The presence of conjunctival petechiae in liv-ing victims of attempted strangulation and experimentally inverted subjects supports our contention that pressure phenomena, not as­phyxia or hypoxia, leads to their development. Moreover, hun-dreds, if not thousands, of persons who have accomplished suicide by placing a plastic bag over their heads, without a concomitant drug overdose, have performed “human experiments” by inducing pure hypoxial deaths. Unless the bag is fastened around the neck by a ligature with sufficient tension to obstruct venous return from the face, in our experience, such persons never have facial or conjunc-tival petechiae. Persons with tight fastenings around the neck are recognizable instantly by their facial plethora and numerous pe-techiae. We are aware that some observers may have seen an occa-sional petechia in rare instances of plastic bag suicide (22). How-ever, we have not seen detailed descriptions of such observations that permit another person to evaluate the variables that might have produced an isolated petechia in a rare victim. Conversely, in New York City, an average of approximately 15 persons per year ac-complish suicide by plastic bag, and we never have observed pe-techiae in a person who did not tightly fasten the bag around his/her neck (19).

The importance of defining the pathogenesis of conjunctival and facial petechiae lies in the potential implications of their misinter-pretation. They are simply markers of increased cephalic venous pressure. In and of themselves, they should not be regarded as sup-portive evidence of asphyxia; in a vacuum, conjunctival and facial petechiae point to no particular cause of death. Only in conjunction with a complete autopsy and thorough death investigation can their potential importance be ascertained, and only with an understand-ing of their pathogenesis can they lend insight into the circum-stances of a death. An erroneous interpretation of this clearly me-chanical phenomenon, which can occur in a heterogenous array of perimortal circumstances, creates a slippery slope. In the best-case scenario, confusion is perpetuated; in the worst-case scenario, the adjudication of criminal cases is severely impaired, and fertile soil having the potential to create false grounds for conviction or ac-quittal is laid.

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  23. CorriveauDM,FritsmaGA.Hemostasisandthrombosisintheclinical laboratory. Philadelphia: Lippincott Company, 1988.

  24. HarmT,RajsJ.Typesofinjuriesandinterrelatedconditionsofvictims and assailants in attempted and homicidal strangulation. Forensic Sci Int 1981 Sep–Oct;18(2):101–23.

Additional information and reprint requests:

Dr. Susan F. Ely

Office of the Chief Medical Examiner of the City of NY

520 First Ave.

New York, NY 10016

Suffocation


  1. Introduction et définition:

  • La suffocation est une asphyxie mécanique, elle est le type de l’asphyxie quasi-pure

  • Elle comprend tous les cas dans lesquels un obstacle mécanique autre que la strangulation, la pendaison et la submersion est apporté violement à l’entrée d’air dans les poumons

  • Elle peut être provoquée par:

    1. L’occlusion directe de la bouche et du nez

    2. L’occlusion des voies aériennes par un corps étranger

    3. La compression thoraco-abdominal

  1. Etiologies:

    1. Obstruction des voies respiratoires:

  • Occlusion au niveau des orifices respiratoires (main, bâillon trop serrée)

  • Obstruction due à un corps étranger, à différents niveau selon sa taille sa forme:

    1. Gros et unique (bol alimentaire chez un vieillard, un glouton- dentaire chez opéré)

    2. Pulvérulent ou visqueux (enfouissement ou enlisement)

    3. Pâteux et plastique (régurgitation du NRS)

    4. Liquide et endogène (œdème aigue du poumon mais on arrive là aux confins de la submersion)

    1. Compression ou perforation de la paroi thoracique:

  1. Par compression externe des parois thoraciques, empêchant toute expansion respiratoire (enlisement)

  2. Par compression interne du ou des poumons, réalisée par un épanchement pleural

  3. Par perforation externe des parois thoraciques

  4. Par perforation interne des poumons

    • Créant dans les deux cas, un pneumothorax dit d’ailleurs « suffocant »

  1. Suffocation par occlusion de la bouche et du nez:

    1. Formes médico-légales:

      1. Crime:

        1. Mode habituel de l’infanticide, par application de la main ou d’un papier humide avec violence occasionnant des lésions de la face

        2. Chez l’adulte vigoureux: la suffocation nécessite une obstruction simultanée de la bouche et du nez, presque toujours le meurtrier complète son acte par une strangulation (difficile chez l’adulte) cependant, la suffocation est plus facile par le maintien de la face contre un sol mou (sable, neige,)

      2. Accident:

          1. Chez l’enfant:

            1. Suffocation faciale du NNE lors de l’accouchement solitaire si la mère perd connaissance

            2. Suffocation faciale du NRS sans le pds de la mère

          2. Chez l’adulte:

            1. Les syncopes, les comas alcooliques ou épileptiques peuvent entraîner la mort par chute face contre un sol mou

            2. Les baillons des sujets en insuffisance respiratoire

            3. Des suffocations dans des sacs en matière plastique (sensation particulière provoquée par l’hypoxie)

      3. Suicide: Il est exceptionnel

    2. Expertise médico-légale:

      1. Examen externe:

              • Met habituellement en évidence:

                1. Une cyanose cervico-faciale

                2. Coloration bleuâtre des ongles et pigmenté hémorragie conjonctivale

              • Le diagnostic de la forme médico-légale repose surtout sur la constatation de signes en rapport avec l’agent suffocant et éventuellement l’existence de celui-ci:

                1. Ecchymoses excoriation de la face de la suffocation faciale du NNE

                2. Baillons en place ou ses traces

                3. Sacs en plastique recouvrant la tête

                4. La mise en évidence de vernis caseors sur un objet de literie à pu, dans quelque cas apporter la preuve d’infanticide par suffocation facial

              • Signe de lutte ou de défense = crime chez l’adulte

      2. Autopsie:

        1. Elle met en évidence une congestion viscérale particulièrement marquée au niveau de poumons

        2. Tache de TARDIEU:

              • Taches sous pleurale lenticulaire, arrondies ou elliptique, plus rarement linéaire et toujours à bords nettement limités de couleur rouge vif, quelque fois brunâtre, leur nombre est variable groupé souvent pré du hile et aux bases,

              • On le rencontre aussi sur les lèvres pariétales et diaphragmatiques et au niveau du péricarde,

              • Résistant longtemps à la putréfaction

        3. Ecchymoses sous pleurale; très évocatrices de suffocation

        4. œdème cérébral

      3. Examens complémentaires:

        1. Histologie pulmonaire: apporte un élément négatif important: absence d’alvéolite

        2. Dosage toxicologique: une alcoolémie élevée, avec une mousse de la longue permet d’étayer l’hypothèse dune suffocation accidentelle par chute en sol mou

  2. Suffocation par obstruction des voies respiratoires par un corps étranger:

    1. Formes médico-légales:

      1. Crime:

        1. C’est un mode fréquent d’infanticide: le tamponnement de l’oropharynx était de nature variée: linge coton hydrophile, papier, mie de pain, paille des cas d’obstruction de flotte au doigt ont été rapportés

        2. Chez l’adulte: il est rare que tells manoeuvre soient exercées

      2. Suicide Il est exceptionnel, (malades mentaux, prisonnier par obstruction du pharynx avec du coton , de la laine,,)

      3. Accident: Les mots accidentels par occlusion du larynx constituent en pratique médico-légale l’immense majorité des suffocations

    2. Suffocations accidentelles par corps étranger chez l’enfant:

Chez le NRS et le jeune enfant c’est la fausse route du bol alimentaire on « embolie de lait » qui est le plus souvent en cause

      1. Physiopathologie:

        1. La mort survient le plus souvent par asphyxie mécanique (obstruction des conduits aériens supérieurs) a ce processus, s’ajoute un phénomène neurovégétatif réflexe à l’origine d’une hypersécrétion bronchique diffuse aux deux poumons, congestion poly viscérale, modifications temporales, et dans certains cas hémorragie méningées

        2. Chez l’enfant de 01 à 05 ans, la suffocation mécanique est le plus souvent le fait d’un objet (bonbons, bille,,,)

      2. Clinique:

        1. Le tableau clinique est dramatique : une dyspnée brutale, souvent suraigu avec tirage sternal intense, angoisse et cyanose

        2. La toux est incessante elle parvient quelque fois à expliquer l’objet ou a le faire tomber dans la trachée

        3. L’œdème et le spasme aggravent rapidement la dyspnée, la laryngoscopie directe s’impose immédiatement, elle permet de voir et d’extraire le corps étranger

        4. En absence d’intervention, après une phase de lutte, l’enfant s’épuise vite, le tirage s’affaiblit, l’enfant livide, meurt une trachéotomie immédiate peut sauver l’enfant

      1. Causes de suffocation médicales:

  • Elles sont non violentes, importante à connaître car à l’origine de mort subite et donc des morts suspectes se sont:

    • Chez le NNé:

      1. Suffocation intra-utérine: inspiration de liquide amniotique

      2. Atrésie du larynx

      3. fistule trachéo-oesophagienne

      4. Kyste de la base du larynx

      5. Atélectasie pulmonaire (obstruction bronchiolaire de matière amniotique)

      6. Pneumonie par inhalation de liquide amniotique

      7. Maladies des membranes hyalines

    • Chez l’enfant:

      1. La croupe (diphtérie)

      2. Laryngite oedémateuse

      3. spasme du larynx

      4. Compression médiastinale

      5. Broncho alvéolites massives

      6. Pneumothorax spontané

      1. Autopsie:

  1. On découvre une obstruction des voies respiratoires trachéo-bronchiolaires par des matières alimentaires de même nature que celles de l’estomac

  2. Présence de alimentaires dans la bouche lorsque la mort est survenue au cours du repas

  3. La dissection montre que les fines divisions bronchiques de 2eme et 3eme division se sont remplis et la pression fait soudre la lumière des bronchioles dans bouchons pâteux et blanchâtres

  4. La section du parenchyme alvéolaire et la pression dans fragments extériorisent des chandelles dans les lumières bronchiques le plus distales

  5. Rhinopharyngite congestion généralisée des viscères

      1. Examens complémentaires: « Examen histologique »:

  1. Présence de substances étrangères obstruant complètement la lumière des branches: petit globules anoxie a des éléments amorphes de couleurs jaunâtre

  2. Mucus abondant: processus obstructif vital

  3. Alvéole rarement atteint par la matière inhalée: aspect d’emphysème avec plages d’œdème + quelque macrophage

  4. Alvéolite réactionnelle: congestion, alvéolite oedémateuse avec macrophage englobant les matière alimentaires à un stade plus avancé: pneumonie réticulée hypertrophique (dans le cas d’une agonie longue avec envahissement des alvéoles)

    1. Suffocation par corps étranger chez l’adulte:

  1. O N retrouve les mêmes types d’accident que chez l’enfant, avec moins de fréquence et plus de variété

  2. Le corps étranger le plus souvent rencontrés sont les bols alimentaires énormes morceaux de viande non-machés ou ayant subie une mastication minime, siègent au niveau du pharynx ou engagés dans la trachée

  3. Il peut s’agir également: dentier, cigare, morceau d’orange

      1. Physiopathologie:

  • La mort est due souvent à l’asphyxie, mais la mort subite est possible

  • Trois principales causes : émotion, ivresse et sénescence l’élément physiopathologique commun étant un trouble de la déglutition

  • Le centre de déglutition voisin du centre respiratoire bulbaire, le pharynx et le larynx participent les 02 à la déglutition et à la ventilation

  • Ils sont reliés à ce noyau par des fibres sensitives et motrices dans le nerf glossopharyngien et pneumogastrique

      1. Causes de suffocation :

  1. Alcool : qui donne une anesthésie des muqueuses du palais et pharynx

  2. Barbituriques : Anesthésie

  3. Antiépileptiques

  4. Emotion

  5. Sénescence (absence de dents, atrophie de la muqueuse et des muscles du pharyngo-oesophagien, déformation

  6. Malformation de l’œsophage

      1. Examen externe et necropsique: Recherche du syndrome asphyxique

      2. Causes de suffocation médicales chez l’adulte:

  1. Inflammation du larynx

  2. Œdème allergique

  3. Tms aggravées par l’inflammation ou les spasmes

  4. Hématome intra pharyngien avec ou sans fracture

  5. Rupture de phlegmon amygdalien ou d’un ganglion caséeux dans une branche

  6. Encombrement trachéo-cranchique

  7. OAP

  8. Etat de mal asthmatique

  9. Embolie pulmonaire

  10. Syndrome bulbaire ; paralysie bilatérale des dilatateurs de la glotte

  11. Coma : fausse route ou stase dans l’apophyse chute de la longue en arrière (Syndrome MENDELSON)

      1. Accidents d’anesthésie:

  1. Les régurgitations : A la phase d’induction de toute anesthésie chez un sujet à estomac plein , anesthésie sans intubation sujet non à jeun au réveil de toute anesthésie

  2. La ptose de la longue : au coma de la période de réveil

  3. Bronchospasme reflexe

Noyade.


NOYADE
DEFINITION : Asphyxie ä, consécutive à une submersion dans un liquide, avec ou sans

inondation broncho-alvéolaire

PHYSIOPATHOLOGIE MODE DE SURVENUE MECANISMES NATURE DU LIQUIDE INHALE
Noyade à « glotte fermée »

– Pc due à l’asphyxie

– laryngospasme définitif, «noyade sèche»

Noyade avec inhalation

– Inondation broncho-alvéolaire

– OAP lésionnel

Hypoxie et hypothermie rapides

Une réanimation prolongée est impérative car l’hypothermie asssu une protection une protection cérébrale relative

On distingue 3 types de noyade :

La noyade par épuisement ou

incapaci

L’hydrocution ou noyadeIIaire

une syncope (thermique, trauma,

allergiq…

La noyade en plongée

(barotraumatisme, accident de

décompression, narcose au mélange, hyperoxye)

re

noyade primaire

sujet conscient alors qu’il

s’enfonce dans l’eau

noyade secondaire

– syncope primitive

. thermodifférentielle

. post-traumatique (choc épigas trique, oculaire, génital)

– Pc : épilepsie, hypoglycémie, TDR  paroxystique

– Accident de plongée

Eau de mer : hypertonique

– majoration de l’inondation

alvéolaire (OAP d’emblée)

– hypovolémie avec hémoconcentration

Eau douce : hypotonique

– Hypervolémie avec hémodilution

– Hémolyse de mécanisme osmoti

que

– Risque cst d’  K+, si inhalation massive

– lésion de la mbr alvéolo-cap et

inactivation du surfactant pulmonaire   micro-atélectasies

SIGNES CLINIQUES
Groupe I

Aquastress

La victime n’a pas inhalé d’eau

Groupe II

Petit hypoxique Inhalation (de l’eau a pénétré dans l’arbre respiratoire), patient«ayant la tasse», toux, cyanose, tachypnée FC rapide, + râles bronchiques, conscience normale

Groupe III

Grand hypoxique OAP et/ou coma, encombrement bturachéo-bronchique grave, detresse respiratoire

Groupe IV

Etat de mort apparente

arrêt circulatoire

Témoigne d’une anoxie durable

CONDUITE A TENIR PREHOSPITALIERE

Dvt un aquastress

Dvt un petit hypoxique

Dvt un grand hypoxique

Etat de mort apparente (réa standard)

asseoir, sécher et frictionner la

(victime essentiellemt encombrée)

– LVAS, aspiration naso-pharyngée – LVAS, VC sous O2 pur et MCE,

victime pour la rechauffer

– rassurer

– étendre, sécher, rechauffer

– aspiration gastrique

– Collier cervical de principe (se méfier d’1 trauma du rachis stt si

SG

– alcalinisation (imp) : bicarb 42%

– contrôler la glycémie et si

– O2 : à hte concentration 8-10l/min coma après plongeon, choc)

20 ml

nécessaire (hypoglycémie) : SG 10% 10 ml en ivl

– sonde gastrique et vidange gastrique

– Respecter axe tête-cou-tronc

– Sécher, rechauffer

– respecter l’hypothermie tant qu’il existe des trbles V° et/ou hémod

– transport médicalisé : en PLS,

– Scope, SpO2, Dynamap, Dextro, T°(protect°céréb) sinon mesures de

Surveillance de 24h dans un

sous O2 à bon débit

– si spasme bronchique :

nébulisation de ventoline (5 mg)

ou Bricanyl + corticoïdes iv

– 02 au masque à fort débit puis

– IOT avec VC (FiO2 100%, PEEP 5-10 mbar si SpO2 basse

ou coma ou VS-PEP si malade en V° spontanée = solution séduisante chez malade en hypoxie modérée)

– Sonde gastrique, vidange gastriqu

lutte contre hypothermie

– prolonger la RCP si il existe une hypothermie

– attention au CEE (assecher le thorax et s’isoler)

centre hospitalier

surveillance 48h dans un service de – 2 vvp + SSI ou macromolécule

soins intensifs du fait d’une

possible aggravation de la fonction respiratoire (OAP secondaire)

(prudence +++) si hypovolémie

(noyade en eau de mer hypertonique) secondaire au

passaged’eau du vaisseau vers l’alvéole : 250 ml en  10 min (à ne pas renouveller car si nécessaire, utiliser amines vasoactives)

– Diurétique si OAP clinique,

noyade en eau douce : Lasilix*

0,5-1 mg/kg (adulte),

1,5-2mg/kg (enfant)

CONDUITE A TENIR INTRA HOSPITALIERE

*Ds les formes graves, grande hypoxie, anoxie: VM+PEP (lutte contre l’hypoxie, CEC (hypothermie prof), correction des troubles hydro- électrolytiques et acido-basique, ATB si eau polluée et septique

*Ds ts les cas : Rx pulm, GDS (  02,  CO2, acidose mixte, Hb (    hémolyse en cas eau douce), K+ (  K+ en cas de mer), EEG et

TDM (si   O2 céréb), swan ganz si SDRA

————————————————————————————————————————————————————————–

LES NOYADES

CHITS O.DUBOIS CS CESU, SAMU 83

CAS 1

• VOUS ÊTES SUR LA PLAGE, VOUS APERCEVEZ UN ATROUPEMENT, VOUS ALLEZ VOIR, VOUS DECOUVREZ UN JEUNE HOMME QUI VIENT D’ÊTRE SORTI DE L’EAU, SOMNOLENT, ENCOMBRE, CYANOSE PERI BUCALE.

• QUEL EST VOTRE ATTITUDE?

DEFINITION

• LA NOYADE  EST UNE ASPHYXIE AIGUE PAR INONDATION BRONCHO- PULMONAIRE, CONSECUTIVE  A UNE IMMERSION OU SUBMERSION. LA QUANTITE  D’EAU N’EST PAS IMPORTANTE, MAIS INHIBE LES ECHANGES GAZEUX ALVEOLO- CAPILLAIRE.

EPIDEMIOLOGIE

• 3000 DECES /AN EN France

• 4EME CAUSE D’ACCIDENT

• 2EME CAUSE DE MORTALITE PAR ACCIDENT, MAIS ELLE EST MAJEURE POUR LES – DE 15ANS

• 17%  DES DECES DES 1-4 ANS

CAUSES DE NOYADE

• SURESTIMATION DE SES CAPACITES

• SOUS ESTIMATION DES RISQUES

• MECONNAISSANCE DU MILIEU

• MAUVAISE UTILISATION DU MATERIEL

• DEFAUT DE SURVEILLANCE

• INCAPACITE DE LAISSER  LA TÊTE HORS DE L’EAU

• INCAPACITE DE REAGIR DANS L’EAU

PHYSIOPATHOLOGIE 1

•    REPOSE SUR 2 ELEMENTS

1. EAU AVALEE

– POSSIBLE D’AVALER DE 2 A5 L

•        DIARRHEE +++

•        EAU + SEL PASSE  DANS LE SANG

•        RISQUE     DE REGURGITATION ET D’INHALATION

PHYSIOPATHOLOGIE 2

2. L’EAU INHALEE

–     DE FAIBLE QUANTITE

–     OEDEME DE LA PAROIE  ALVEOLAIRE DU A LA DESTRUCTION DU SURFACTANT

IMPOSSIBILITE D’ECHANGES GAZEUX

PHYSIOPATHOLOGIE 3

•    LES CONSEQUENCES  DE L’IMMERSION

–     3 STADES

1.  SPASME: EAU           SPASME LARYNGE

2.  DEGLUTITION: HYPOXIE              DEGLUTITION REFLEXE SOUS L’EAU

3.  INHALATION:               SPASME LARYNGE INSPIRATION EN IMMERSION

DANS 10%  DES CAS LE SPASME  LARYNGE PERSISTE                           NOYADE  A POUMONS SECS

INFLUENCE DE LA NATURE  DE L’EAU

1.  EAU DOUCE:

Na Cl EAU DOUCE  < Na Cl  SANG

EAU PASSE  DANS LA CIRCULATION SURCHARGE VASC                                INSUFF CARDIAQUE

2 .  EAU DE MER:

Na Cl EAU MER > Na Cl SANG

FUITE LIQUIDIENNE DU SANG  A TRAVERS  LA PAROIE ALVEOLO CAPILLAIRE                  OAP

MECANISMES ET SIGNES 1

•    DEUX TYPES DE NOYADE

1. NOYADE PRIMAIRE ASPHYXIQUE

« NOYADE BLEUE, VRAIE NOYADE »

2. NOYADE SECONDAIRE SYNCOPALE

« NOYADE BLANCHE, FAUSSE NOYADE »

MECANISMES ET SIGNES 2

1. NOYADE ASPHYXIQUE

SE PRODUIT EN CINQ PHASES:

–     1) AGITATION        ( MVT DE BOUCHON)

–     2) APNEE REFEXE ( GLOTTE FERMEE)

–     3) REPRISE DE LA RESPIRATION (EAU)

–     4) CONVULSIONS (HYPOXIE, HYPERCO2)

–     5) MORT

MECANISMES ET SIGNES 3

1.1  NOYADE ASPHYXIQUE QUATRE STADES DE GRAVITE A) STADE 1: L’AQUASTRESS

–     UN PEU D’EAU AVALEE

–     N:CONSCIENCE                NORMALE

–     R:RESPIRATION               NORMALE

–     C:CIRCULATION              NORMALE

–     PERSONNE ANGOISSEE, FROIDE, EPUISEE

–     CAT: RECHAUFFER, RASSURER, O2, SURVEILLANCE A L’HÔPITAL

MECANISMES ET SIGNES 4

B) STADE 2 : PETIT HYPOXIQUE

– EAU AVALEE, LEGERE INHALATION

– N:CONSCIENCE                 NORMALE

– R:RESPIRATION                 PETITE GÊNE

– C:CIRCULATION                NORMALE

– PERSONNE ENCOMBREE, FROIDE, EPUISEE, ANXIEUSE

– CAT: RECHAUFFER, RASSURER, O2, PERF,LIBERER VAS, SURVEILLANCE SaO2,  POULS, TA, ASPIRATION DIGESTIVE, CONSCIENCE.

MECANISMES ET SIGNES 5

C) STADE 3: GRAND HYPOXIQUE

– EAU AVALEE +++, INHALATION+

– N:CONSCIENCE           SOMNOLENCE /AGITE

– R:RESPIRATION           ENCOMBREMENT +++, CYANOSE DES LEVRES, EXTREMITES (BLEU)

– C:CIRCULATION           TACHYCARDIE

– ESTOMAC PLEIN              RISQUE D’INHALATION SUP

MECANISMES ET SIGNES 6

CONDUITE  A TENIR STADE 3

URGENCE

LIBERER VAS, ASPIRATION DIGESTIVE, O2

HT CONCENTRATION, PREPARER IOT, PERF, RECHAUFFER, SURVEILLANCE CONSCIENCE  +++, SaO2, POULS, TA, BILAN SANG : IONO, NFS, GDS …..

MECANISMES ET SIGNES 7

D) STADE 4: ANOXIQUE

– EAU +++ DANS L’ESTOMAC ET POUMONS

– CONSCIENCE         COMA

– RESPIRATION                NULLE

– CIRCULATION               POULS FILANT /ARRET

– ETAT DE MORT APPARENTE

MECANISMES ET SIGNES 8

CONDUITE  A TENIR STADE 4

URGENCE +++

LIBERER VAS, IOT, ASPIRATION GASTRIQUE, PERF, RCP AVEC MCE, AMINE PRESSIVE, DIURESE (Sondage),

SURVEILLANCE DES CONSTANTES, TTT DE L’OAP …..

MECANISMES ET SIGNES 9

2. NOYADE SYNCOPALE

LA SYNCOPE  EST PRIMITIVE  AVANT DE TOMBER DANS L’EAU:                   PAS DE CYANOSE

–     N:CONSCIENCE           COMA

–     R:RESPIRATION           FAIBLE OU NULLE

–     C:CIRCULATION           ARRET

–     CAT: cf ARRET CARDIAQUE, INTERROGER POUR CONNAÎTRE LES ATCD

CONCLUSION

• SORTIR RAPIDEMENT  LA VICTIME  DE L’EAU

• BILAN CLINIQUE +++

• ENGAGEMENT DE LA RCP +++

• SI NON RECHAUFFER, RASSURER, SURVEILLER.

CAS 1

• VOUS ÊTES SUR LA PLAGE, VOUS APERCEVEZ UN ATROUPEMENT, VOUS ALLEZ VOIR, VOUS DECOUVREZ UN JEUNE HOMME QUI VIENT D’ÊTRE SORTI DE L’EAU, SOMNOLENT, ENCOMBRE, CYANOSE PERI BUCALE.

• QUEL EST VOTRE ATTITUDE?

CAS 2

• VOUS ÊTES SUR UNE BARGE DE PLONGEE SOUS MARINE, ON VOUS PREVIENT

QU’UN PLONGEUR EST INCONSCIENT SOUS L’EAU,IL EST RAMENE  A LA SURFACE.

• QUEL EST VOTRE REFLEXION, VOS PREPARATIONS POUR ACCEUILLIR  LE PLONGEUR  A SA SORTIE DE L’EAU?