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Experimental evaluation of rigor mortis. VI. Effect of various causes of death on the evolution of rigor mortis
Forensic Science International, 22 (1983) Elsevier Scientific Publishers Ireland Ltd.
1
l-9
EXPERIMENTAL EVALUATIONOF RIGOR MORTIS. VI. EFFECT OF VARIOUS MORTIS
CAUSES
T. KROMPECHER,
OF
C. BERGERIOUX,
Institute of Forensic Medicine, Lausanne (Switzerland) (Received (Revision (Accepted
DEATH
ON
THE
EVOLUTION
C. BRANDT-CASADEVALL
OF RIGOR
and H.-R. GUJER
University of Lausanne, Rue Char-Roux
29/31,
CH-1005
June 7, 1982) received October 18, 1982) November 9,1982)
Summary The evolution of rigor mortis was studied in cases of nitrogen asphyxia, drowning and strangulation, as well as in fatal intoxications due to strychnine, carbon monoxide and curariform drugs, using a modified method of measurement. Our experiments demonstrated that: (1) (2) (3) (4)
Strychnine intoxication hastens the onset and passing of rigor mortis. CO intoxication delays the resolution of rigor mortis. The intensity of rigor may vary depending upon the cause of death. If the stage of rigidity is to be used to estimate the time of death, it is necessary: (a) to perform a succession of objective measurements of rigor mortis intensity; and (b) to verify the eventual presence of factors that could play a role in the modification of its development.
Key words: Rigor mortis;
Experimentation;
Intoxication;
Asphyxia;
Time of death
Introduction Rigor mortis has always been considered as an important means of the estimation of the time of death. It is also generally admitted that different factors - intrinsic as well as extrinsic - may influence its development. We consider that these factors are: (1) Preceding
death :
(a) in direct relatio,i to the cause of death (such as a fatal intoxication); (b) without any relation to the cause of death (such as violent exertion shortly before death resulting from another cause). 0379~0738/83/$03.00
o Elsevier Scientific Publishers Ireland Printed and Published in Ireland
Ltd.
2
(2) Following death : for example: ambient
temperature,
mechanical
break of rigidity,
etc.
4 review of literature published between 1811 and 1960 and dealing with chronological data of development of rigor mortis shows estimations varying within very large limits [ 11. For example, resolution was reported to occur from 44 hpm to 108 hpm according to different authors. We assume that these great differences have two principal causes: (1) the development of rigor mortis depends on many factors pre- and post mortem; and (2) all statements emitted about the state of rigidity are based on subjective judgements. Several authors studied the possible influence of various factors on rigor mortis in order to avoid errors of estimation due to changes induced by such factors. They established - in animal experiments - that chloroform, ether or chloralhydrate delay the onset of rigor mortis [2]. Pentachlorphenol, on the contrary, hastens its development [ 31. It was also reported that th,e ir~b,ibit;or, of &olmesterase hms~~r,s tp,e orlset of rigor niortis by 9.5.zl.5 h as compared to controls, whereas atropine has the opposite effect [4]. Others studied the influence of temperature in animal experiments [3,5] or on humans [ 31. The results mentioned above were - with one exception [ 33 - obtained by subjective estimations. More recently, several authors published results based on objective measurements. For example Zink [6,7] investigated the mechanical properties of fresh and rigid human skeletal muscle fibers and whole muscles by measurement of the tensile forces. Other authors have ‘determined the torque necessary to break rigor mortis in a human cadaver in order to estimate the time of death [ 81 or the maximum laytime [ 9,101. These publications give important information about the rigor mortis but the method of a single measurement does not allow its development to be followed. In our previous experiments [ 11,121 we studied and quantified the effect of physical exercise before death (group lb) and of ambient temperature (group 2) on its evolution, using a method permitting objeotive and serial measurements of its intensity. In the present study, the possible influence of causes of death (group la) was investigated. Materials andmethods ELnn~im~ntc rmyr?LllllTjllw
xxrnra ““r;l.z nnnArlc+nA L”IIULI~YC;U
nrcino UULU~ Ql3 V” mnln IIILu\;
nlhinn CyUll,”
mta (atvnin aLLu.2\““IcuIA
QTV5? nf WI. Y “1
the ‘Institut fiir Zuchthygiene’, University of Zurich), weighing 305 f 15 g. They were divided into eight groups of ten rats, in order to ensure a homogeneous repartition of the animals’ individual weights, They were always killed at the same time of day (between 08 :00 and 09 :00 h) without any previous treatment.
3
In the first series, performed on four rats were killed in the following way:
groups
of ten animals
each, the
Group 1: Nitrogen asphyxia (in a dessicator purged with a flow of nitrogen) - death within approx. 2 min. Group 2: Drowning (the animals were maintained in tepid water, 28°C) - death within 2-3 min. Group 3: Ether overdose - death within approx. 4-6 min. Group 4: Strangulation by means of a small cord - death within approx. 2 min. In the second series, also performed on four groups of ten animals each, the rats were killed in the following way: Group 1: Nitrogen asphyxia (identical to the preceding group 1, in order to be able to compare the results of the two series). Group 2: Intraperitoneal injection of strychnine (3.75 mg/kg - five times the lethal dose) - death within approx. 10 min. Group 3: Carbon monoxide intoxication (two successive injections of 20 cm3 of pure carbon monoxide at lo-min intervals in a 6.2 1 closed dessicator containing 3 rats) - death 2-3 min after the second injection. An estimation of carboxyhemoglobin saturation level was performed on two rats. The results were 87% and 89% saturation. Group 4: Intraperitoneal injection of 50 mg of suxamethonium chloride (Mydarine) - death within approx. 2 min. After death, the rats were immediately placed in the measuring apparatus already described in detail elsewhere [ 13, 141. In the present study, a modification of the previously used method of measurement was performed. This modification does not affect the general principle which is the measurement of the force necessary to cause a movement of small amplitude (4 mm) of the hind limbs, a test that does not break rigor mortis but allows serial measurements. Actually it is a new system permitting a more efficient and rapid determination of the force: in the previous technique, as shown in Fig. l(c), the measurement of this force was achieved by hooking successively increasing weights in order to obtain the standardised movement of the limb. However, the hook is now attached to the plate of a digital balance (see d on Fig. 1) which is nlnod en g jzck. Whew the hPlannn in te y*wvuUc&AUI4bL.k I” ~AW~FLA I”..~~cIU 111 nwlnr “IUCI produce the standardised small-amplitude movement of the limb, the resistance due to rigidity can be read directly (as a negative value since it is a traction). Readings were performed after a delay of 5 s. The ambient temperature was 24 + 0.5’C. For statistical analysis of the results, the Student t-test was used.
Fig. 1. Apparatus for the measurement of rigor mortis intensity: (a) cord attached to hind limb; (b) steel hooks permitting attachment of cord to limbs; (c) hook supporting weights (previous technique); (d) hook attached to a digital balance.
Results and discussion We compared curves of rigor mortis in the case of ether overdose obtained with the previous [ 11,12,14,15] and new methods of measurement. We found that the chronology of rigor development remained unchanged; the curves have identical shape. First series of experiments The results of the first series are presented in Table 1 and Fig. 2. It is obvious that the general shape of the four curves is quite similar - beginning with an abrupt rise and reaching a maximum value between 5 h and 6 h post-mortem (hereafter referred to as hpm) in the nitrogen, ether and drowning groups, and between 5 and 8 hpm in the strangulation group. This indicates that these curves present a plateau rather than a peak as maximal value. The first statistically significant decrease with reference to the maximal value occurs at 8 hpm for the nitrogen (P < 0.025), ether (P < 0.005) and drowning (P < 0.01) groups and at 10 hpm for the strangulation group
5 TABLE 1 INTENSITY CHANGES OF RIGOR MORTIS IN THE HIND LIMBS OF RATS DURING ITS EVOLUTION DUE TO VARIOUS CAUSES OF DEATH Mean values (in grams) for 10 animals (20 hind limbs). Consecutive values show a difference statistically significant (P < 0.05) expecting the cases where there is a symbol ” between them. 1
ITlLl_
rme yosr-
mortem
l?J
(h)
-
_..
mer
overdose
2 4 5
35.1 47.5 54.6 I,
28.0 43.3 46.5 ,,
23.6 37.7 45.3 ,,
30.4 47.3 51.5 8,
6
52.8
43.8
45.0
53.1
8 10 12 24
49.5
39.6
40.6 33.1 23.3
31.8 27.6 24.0
40.7 33.7 28.8 20.0
5i.7 39.3 33.6 24.3
weight
I grams
t #me I hours Fig. 2. Evolution of rigor mortis in t&e hind limbs of rats in the case of: -: nitrogen asphyxia; . . . . . . . . . . . . . . . . drowning; ----: ether overdose; ---a---: strangulation. Meanvalues for 10 animals (20 hind limbs).
6
(P < 0.0005). The resolution of the rigidity is rather important up to 12 hpm. The decrease is statistically significant between 8 and 10 hpm and 10 and 12 hpm in each group. After 12 hpm, the changes become less and less significant. It is also interesting to note that the curves of the nitrogen and strangulation groups are significantly higher than those of the ether and drowning groups (P < 0.05), demonstrating that rigor intensity is higher in the two first groups. The difference between these groups remains statistically significant at 8, 10 and 12 hpm. Second series of experiments In this series of experiments, we compared the influence of lethal strychnine, carbon monoxide and curariform drug intoxication on the development of rigor mortis. In a preliminary experiment, we compared the influence of two types of curariform drugs, Mydarinee (Welcome) and Pavulon@ (Organon), respectively a depolarizing (suxamethonium chloride) and a non-depolarizing (pancuronium bromide) agent. The experiment was performed on two groups of three animals each. No significant differences were found in the development and intensity of rigor in the two urn1 1nr -*v-y”.
-PnrVA
nrnrtiral r*..,-“_--
suxamethonium weight
rcamns___) __-_
ip_ this -I-_-
savwwl --_____
swim --_---,
wp
&~ge
t,n 1~s~ the
chloride.
/grams
01
2
4
5
6
6
12
16
24 tvmelhours
Fig. 3. Evolution of rigor mortis in the hind limbs of rats in the case of: -: nitrogen carbon monoxide; -*-: asphyxia; . . . . . . . . . . . . fatal intoxication by strychnine; -----: curare. Mean-values for 10 animals (20 hind limbs).
xdnoti aaxxn3 put? 03 aq? 30 asoy uey~ (90.0 > a) ra@y dpu~x3 -!tijs an? sdnoti a+.u.@~~s putz ua3oq~u aq$ u! sanpn @~xtxu ay,~ ‘p!dw ssa~ s! &~p$+ a% 30 uoyyosaJ aqq ‘dnozflo3 aqq30 as’t23aql UI ‘sdnofi (z;o’o > a) 03 pm (sooo*o > d) aJeln3 ‘(~OOO’O > a) ua2ow ay7 103 urdy 8 lx? :(~OOO’O > a) dnoti ayuyD&s aq$ ~03 wdy p qt3 sJn330 anpA ~uynxu aqq 09 axara3ar u! astzaI%p ~utz~~3ytl~s 7szi3 ay& *dnoti 03 aq$ ~03 urdy g 3~ pun sdno&i ua?loqy prne anxn3 aw ~03 urdy g pue g uaaM?aq fdnoti au~uy~A~~s ayl ~03 tudy z qtz payz?aJ ST anpA uxnuryxu ay& ‘Iauoos 61~uwgyu$s nzaddB syotu ro%y 30 uoynlosaz puv qasuo ay& ‘$3al aqq 09 pa?~!ys aq 07 snzadde (a~uycA.t~s) dnoti puoaas aqg 30 ahltw ay& *sapas 9~x3 ay7 30 ?E~F)03 nz[!ury s! sahxn3 aql30 adeys FrauaS ayL
-
-
-
-
:aptxu aq u~3 syawual fl~~o~~o3
6’02
P’9Z
9’OZ
0’9Z
PZ
P’ZE P’OP L’O9 Z’99
91
B’PZ
L*iB
E’IZ
P’6Z 8’96
0’98
O’LP
9’9P
6’6Z 8’82 P’98
I& Z’W 8’82
Z’8P
O.&P
6’8fi I’LZ
ZT
8 9 9 P Z 1
‘way* uaahwq ,, Ioqm6s e s! aray? azaym sasm ay$ ifu!ldaoxa (90.0 > d) aagaag!u%!s XIIE~!~S!~E$Sama -JaJgp e fioqs satyea aagnaasuo3 ‘(squr!I pu!q OZ) sp3ugm 01 103 (swtlr%u!) saysa uaam
H,LVBCId0 SBSflV3 SflOIXVA OIL3MI NOIUl?Oh3 SU 3NIZIIlCI SkVX iI0 SWWI CINIH3HJ2 NI SLLllOk’I zIOE)IX d0 S33NVH3 LLISNBLLNI z 3lEIVL L
8
group and an increase in the CO group since the maximum value is not yet attained. At 6, 8, 12 and 16 hpm, a total inversion of the situation is observed: the values of the CO group are higher; the differences are statistically significant (P < 0.001). This comparison shows that a succession of objective measurements is essential to evaluate the stage of rigidity. At the same time, our experiments also revealed that certain intoxications may have an influence on the development of rigor mortis, in agreement with published data [2-41. Very important differences can be found when comparing groups or individuals influenced by different factors in which some have an opposite effect on the evolution of rigor mortis. For the present, we can only report on the phenomena without being able to give a reasonable explanation, Take for example the case of lethal strychnine intoxication where violent cramps precede death. According to present knowledge, the onset of rigor mortis is due to a lack of ATP. Therefore, it is supposed that the accelerated apparition of the rigidity is the consequence of the quantitative decrease of the available ATP due to intense muscle activity. This explanation would be quite satisfactory but what is the relationship with the accelerated resolution also seen in this case? Furthermore, this same phenomenon was not found in the case of physical exercise preceding death [ 111. There is no explanation for the significant increase in the intensity of rigor mortis in some cases, nor for the slower resolution in the CO group. We do not know to what extent our findings are directly valid for humans. Considering the great similarity of mammalian muscle tissues, we can, however, suppose that the same tendency exists for man. According to our present results, we propose that, if the stage of rigidity is to be used as a means to estimate the time of death, it is necessary: (1) to of (2) to its
perform a succession of objective measurements of the intensity rigor mortis; and verify the eventual presence of factors that could play a role in development.
Acknowledgement The authors wish to express their thanks to Mrs. E. Haller, from the Department of Medical Statistics, Institute of Social and Preventive Medicine, University of Lausanne (Switzerland), for the statistical analysis. References 1 H.J. Mallach and H.-J. Mittmeyer, Totenstarre und Totenflecke. 2. Rechtsmed., 69 (1971) 70-78. 2 M. Bierfreund, Untersuchungen iiber die Todtenstarre. Pfliigers Arch. ges. Physiol., 43 (1888) 195-216.
9
3 B. Forster, D. Ropohl, 0. Prokop and K. Riemer, Tierexperimentelle und an menschlichen Leichen gewonnene Daten zur Frage der Dauer der Totenstarre. Krim. Forensische Wk., 13 (1974) 35-45. 4 S.P. Berg, Nervensystem und Totenstarre. Dtsch. 2. Gesamte Gerichtl. Med., 39 (1948/1949) 429-434. 5 S. Morgenstern, Experimentelle Ergebnisse zur Frage des Temperatureinflusses auf die Leichenstarre. Dtsch. 2. Gesamte Gerichtl. Med., 9 (1927) 718-722. 6 P. Zink, Mechanische Eigenschaften lebensfrischer und totenstarrer menschlicher Skeletmuskelfasern und ganzer Muskeln. 2. Rechtsmed., 70 (1972) 163-177. 7 P. Zink, Uber das Verhalten des menschlichen Skeletmuskels bei Dehnung wlhrend des Verlaufs der Totenstarre. Habilitationsschrift, Erlangen-Niirnberg, 1970. 8 B. Forster, D. Ropohl and P. Raule, Eine neue Formel zur Beurteilung der Totenstarre: Die Feststellung des FRR-Index. 2. Rechtsmed., 80 (1977) 51-54. 9 G. Beier, E. Liebhardt, M. Schuck and W. Spann, Totenstarremessungen an menschlichen Skelettmuskeln in situ. 2. Rechtsmed., 79 (1977) 277-283. 10 M. Schuck, G. Beier, E. Liebhardt and W. Spann, Zur Schiitzung der Liegezeit durch Messungen der Totenstarre. Beitr. Gerichtl. Med., 36 (1978) 339.-343. 11 T. Krompecher and 0. Frye, Experimental evaluation of rigor mortis. IV. Change in strength and evolution of rigor mortis in the case of physical exercise preceding death. Forensic Sci. Znt., 12 (1978) 103-107. 12 T. Krompecher, Experimental evaluation of rigor mortis. V. Effect of various temperatures on the evolution of rigor mortis. Forensic Sci. Znt., 17 (1981) 19-26. 13 T. Krompecher and 0. Frye, Experimentelle Untersuchungen an der Leichenstarre. II. Das Entstehen der Leichenstarre unter Einfluss von korperlicher Anstrengung. Beitr. Gerichtl. Med., 36 (1978) 345-349. 14 T. Krompecher and 0. Frye, Experimental evaluation of rigor mortis. III. Comparative study of the evolution of rigor mortis in different sized muscle groups in rats. Forensic Sci. Znt., 12 (1978) 97-102. 15 T. Krompecher and 0. Frye, Zur Frage der Todeszeitbestimmung aufgrund der Leichenstarre. Beitr. Gerichtl. Med., 37 (1979) 285-289.
1
l-9
EXPERIMENTAL EVALUATIONOF RIGOR MORTIS. VI. EFFECT OF VARIOUS MORTIS
CAUSES
T. KROMPECHER,
OF
C. BERGERIOUX,
Institute of Forensic Medicine, Lausanne (Switzerland) (Received (Revision (Accepted
DEATH
ON
THE
EVOLUTION
C. BRANDT-CASADEVALL
OF RIGOR
and H.-R. GUJER
University of Lausanne, Rue Char-Roux
29/31,
CH-1005
June 7, 1982) received October 18, 1982) November 9,1982)
Summary The evolution of rigor mortis was studied in cases of nitrogen asphyxia, drowning and strangulation, as well as in fatal intoxications due to strychnine, carbon monoxide and curariform drugs, using a modified method of measurement. Our experiments demonstrated that: (1) (2) (3) (4)
Strychnine intoxication hastens the onset and passing of rigor mortis. CO intoxication delays the resolution of rigor mortis. The intensity of rigor may vary depending upon the cause of death. If the stage of rigidity is to be used to estimate the time of death, it is necessary: (a) to perform a succession of objective measurements of rigor mortis intensity; and (b) to verify the eventual presence of factors that could play a role in the modification of its development.
Key words: Rigor mortis;
Experimentation;
Intoxication;
Asphyxia;
Time of death
Introduction Rigor mortis has always been considered as an important means of the estimation of the time of death. It is also generally admitted that different factors - intrinsic as well as extrinsic - may influence its development. We consider that these factors are: (1) Preceding
death :
(a) in direct relatio,i to the cause of death (such as a fatal intoxication); (b) without any relation to the cause of death (such as violent exertion shortly before death resulting from another cause). 0379~0738/83/$03.00
o Elsevier Scientific Publishers Ireland Printed and Published in Ireland
Ltd.
2
(2) Following death : for example: ambient
temperature,
mechanical
break of rigidity,
etc.
4 review of literature published between 1811 and 1960 and dealing with chronological data of development of rigor mortis shows estimations varying within very large limits [ 11. For example, resolution was reported to occur from 44 hpm to 108 hpm according to different authors. We assume that these great differences have two principal causes: (1) the development of rigor mortis depends on many factors pre- and post mortem; and (2) all statements emitted about the state of rigidity are based on subjective judgements. Several authors studied the possible influence of various factors on rigor mortis in order to avoid errors of estimation due to changes induced by such factors. They established - in animal experiments - that chloroform, ether or chloralhydrate delay the onset of rigor mortis [2]. Pentachlorphenol, on the contrary, hastens its development [ 31. It was also reported that th,e ir~b,ibit;or, of &olmesterase hms~~r,s tp,e orlset of rigor niortis by 9.5.zl.5 h as compared to controls, whereas atropine has the opposite effect [4]. Others studied the influence of temperature in animal experiments [3,5] or on humans [ 31. The results mentioned above were - with one exception [ 33 - obtained by subjective estimations. More recently, several authors published results based on objective measurements. For example Zink [6,7] investigated the mechanical properties of fresh and rigid human skeletal muscle fibers and whole muscles by measurement of the tensile forces. Other authors have ‘determined the torque necessary to break rigor mortis in a human cadaver in order to estimate the time of death [ 81 or the maximum laytime [ 9,101. These publications give important information about the rigor mortis but the method of a single measurement does not allow its development to be followed. In our previous experiments [ 11,121 we studied and quantified the effect of physical exercise before death (group lb) and of ambient temperature (group 2) on its evolution, using a method permitting objeotive and serial measurements of its intensity. In the present study, the possible influence of causes of death (group la) was investigated. Materials andmethods ELnn~im~ntc rmyr?LllllTjllw
xxrnra ““r;l.z nnnArlc+nA L”IIULI~YC;U
nrcino UULU~ Ql3 V” mnln IIILu\;
nlhinn CyUll,”
mta (atvnin aLLu.2\““IcuIA
QTV5? nf WI. Y “1
the ‘Institut fiir Zuchthygiene’, University of Zurich), weighing 305 f 15 g. They were divided into eight groups of ten rats, in order to ensure a homogeneous repartition of the animals’ individual weights, They were always killed at the same time of day (between 08 :00 and 09 :00 h) without any previous treatment.
3
In the first series, performed on four rats were killed in the following way:
groups
of ten animals
each, the
Group 1: Nitrogen asphyxia (in a dessicator purged with a flow of nitrogen) - death within approx. 2 min. Group 2: Drowning (the animals were maintained in tepid water, 28°C) - death within 2-3 min. Group 3: Ether overdose - death within approx. 4-6 min. Group 4: Strangulation by means of a small cord - death within approx. 2 min. In the second series, also performed on four groups of ten animals each, the rats were killed in the following way: Group 1: Nitrogen asphyxia (identical to the preceding group 1, in order to be able to compare the results of the two series). Group 2: Intraperitoneal injection of strychnine (3.75 mg/kg - five times the lethal dose) - death within approx. 10 min. Group 3: Carbon monoxide intoxication (two successive injections of 20 cm3 of pure carbon monoxide at lo-min intervals in a 6.2 1 closed dessicator containing 3 rats) - death 2-3 min after the second injection. An estimation of carboxyhemoglobin saturation level was performed on two rats. The results were 87% and 89% saturation. Group 4: Intraperitoneal injection of 50 mg of suxamethonium chloride (Mydarine) - death within approx. 2 min. After death, the rats were immediately placed in the measuring apparatus already described in detail elsewhere [ 13, 141. In the present study, a modification of the previously used method of measurement was performed. This modification does not affect the general principle which is the measurement of the force necessary to cause a movement of small amplitude (4 mm) of the hind limbs, a test that does not break rigor mortis but allows serial measurements. Actually it is a new system permitting a more efficient and rapid determination of the force: in the previous technique, as shown in Fig. l(c), the measurement of this force was achieved by hooking successively increasing weights in order to obtain the standardised movement of the limb. However, the hook is now attached to the plate of a digital balance (see d on Fig. 1) which is nlnod en g jzck. Whew the hPlannn in te y*wvuUc&AUI4bL.k I” ~AW~FLA I”..~~cIU 111 nwlnr “IUCI produce the standardised small-amplitude movement of the limb, the resistance due to rigidity can be read directly (as a negative value since it is a traction). Readings were performed after a delay of 5 s. The ambient temperature was 24 + 0.5’C. For statistical analysis of the results, the Student t-test was used.
Fig. 1. Apparatus for the measurement of rigor mortis intensity: (a) cord attached to hind limb; (b) steel hooks permitting attachment of cord to limbs; (c) hook supporting weights (previous technique); (d) hook attached to a digital balance.
Results and discussion We compared curves of rigor mortis in the case of ether overdose obtained with the previous [ 11,12,14,15] and new methods of measurement. We found that the chronology of rigor development remained unchanged; the curves have identical shape. First series of experiments The results of the first series are presented in Table 1 and Fig. 2. It is obvious that the general shape of the four curves is quite similar - beginning with an abrupt rise and reaching a maximum value between 5 h and 6 h post-mortem (hereafter referred to as hpm) in the nitrogen, ether and drowning groups, and between 5 and 8 hpm in the strangulation group. This indicates that these curves present a plateau rather than a peak as maximal value. The first statistically significant decrease with reference to the maximal value occurs at 8 hpm for the nitrogen (P < 0.025), ether (P < 0.005) and drowning (P < 0.01) groups and at 10 hpm for the strangulation group
5 TABLE 1 INTENSITY CHANGES OF RIGOR MORTIS IN THE HIND LIMBS OF RATS DURING ITS EVOLUTION DUE TO VARIOUS CAUSES OF DEATH Mean values (in grams) for 10 animals (20 hind limbs). Consecutive values show a difference statistically significant (P < 0.05) expecting the cases where there is a symbol ” between them. 1
ITlLl_
rme yosr-
mortem
l?J
(h)
-
_..
mer
overdose
2 4 5
35.1 47.5 54.6 I,
28.0 43.3 46.5 ,,
23.6 37.7 45.3 ,,
30.4 47.3 51.5 8,
6
52.8
43.8
45.0
53.1
8 10 12 24
49.5
39.6
40.6 33.1 23.3
31.8 27.6 24.0
40.7 33.7 28.8 20.0
5i.7 39.3 33.6 24.3
weight
I grams
t #me I hours Fig. 2. Evolution of rigor mortis in t&e hind limbs of rats in the case of: -: nitrogen asphyxia; . . . . . . . . . . . . . . . . drowning; ----: ether overdose; ---a---: strangulation. Meanvalues for 10 animals (20 hind limbs).
6
(P < 0.0005). The resolution of the rigidity is rather important up to 12 hpm. The decrease is statistically significant between 8 and 10 hpm and 10 and 12 hpm in each group. After 12 hpm, the changes become less and less significant. It is also interesting to note that the curves of the nitrogen and strangulation groups are significantly higher than those of the ether and drowning groups (P < 0.05), demonstrating that rigor intensity is higher in the two first groups. The difference between these groups remains statistically significant at 8, 10 and 12 hpm. Second series of experiments In this series of experiments, we compared the influence of lethal strychnine, carbon monoxide and curariform drug intoxication on the development of rigor mortis. In a preliminary experiment, we compared the influence of two types of curariform drugs, Mydarinee (Welcome) and Pavulon@ (Organon), respectively a depolarizing (suxamethonium chloride) and a non-depolarizing (pancuronium bromide) agent. The experiment was performed on two groups of three animals each. No significant differences were found in the development and intensity of rigor in the two urn1 1nr -*v-y”.
-PnrVA
nrnrtiral r*..,-“_--
suxamethonium weight
rcamns___) __-_
ip_ this -I-_-
savwwl --_____
swim --_---,
wp
&~ge
t,n 1~s~ the
chloride.
/grams
01
2
4
5
6
6
12
16
24 tvmelhours
Fig. 3. Evolution of rigor mortis in the hind limbs of rats in the case of: -: nitrogen carbon monoxide; -*-: asphyxia; . . . . . . . . . . . . fatal intoxication by strychnine; -----: curare. Mean-values for 10 animals (20 hind limbs).
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8
group and an increase in the CO group since the maximum value is not yet attained. At 6, 8, 12 and 16 hpm, a total inversion of the situation is observed: the values of the CO group are higher; the differences are statistically significant (P < 0.001). This comparison shows that a succession of objective measurements is essential to evaluate the stage of rigidity. At the same time, our experiments also revealed that certain intoxications may have an influence on the development of rigor mortis, in agreement with published data [2-41. Very important differences can be found when comparing groups or individuals influenced by different factors in which some have an opposite effect on the evolution of rigor mortis. For the present, we can only report on the phenomena without being able to give a reasonable explanation, Take for example the case of lethal strychnine intoxication where violent cramps precede death. According to present knowledge, the onset of rigor mortis is due to a lack of ATP. Therefore, it is supposed that the accelerated apparition of the rigidity is the consequence of the quantitative decrease of the available ATP due to intense muscle activity. This explanation would be quite satisfactory but what is the relationship with the accelerated resolution also seen in this case? Furthermore, this same phenomenon was not found in the case of physical exercise preceding death [ 111. There is no explanation for the significant increase in the intensity of rigor mortis in some cases, nor for the slower resolution in the CO group. We do not know to what extent our findings are directly valid for humans. Considering the great similarity of mammalian muscle tissues, we can, however, suppose that the same tendency exists for man. According to our present results, we propose that, if the stage of rigidity is to be used as a means to estimate the time of death, it is necessary: (1) to of (2) to its
perform a succession of objective measurements of the intensity rigor mortis; and verify the eventual presence of factors that could play a role in development.
Acknowledgement The authors wish to express their thanks to Mrs. E. Haller, from the Department of Medical Statistics, Institute of Social and Preventive Medicine, University of Lausanne (Switzerland), for the statistical analysis. References 1 H.J. Mallach and H.-J. Mittmeyer, Totenstarre und Totenflecke. 2. Rechtsmed., 69 (1971) 70-78. 2 M. Bierfreund, Untersuchungen iiber die Todtenstarre. Pfliigers Arch. ges. Physiol., 43 (1888) 195-216.
9
3 B. Forster, D. Ropohl, 0. Prokop and K. Riemer, Tierexperimentelle und an menschlichen Leichen gewonnene Daten zur Frage der Dauer der Totenstarre. Krim. Forensische Wk., 13 (1974) 35-45. 4 S.P. Berg, Nervensystem und Totenstarre. Dtsch. 2. Gesamte Gerichtl. Med., 39 (1948/1949) 429-434. 5 S. Morgenstern, Experimentelle Ergebnisse zur Frage des Temperatureinflusses auf die Leichenstarre. Dtsch. 2. Gesamte Gerichtl. Med., 9 (1927) 718-722. 6 P. Zink, Mechanische Eigenschaften lebensfrischer und totenstarrer menschlicher Skeletmuskelfasern und ganzer Muskeln. 2. Rechtsmed., 70 (1972) 163-177. 7 P. Zink, Uber das Verhalten des menschlichen Skeletmuskels bei Dehnung wlhrend des Verlaufs der Totenstarre. Habilitationsschrift, Erlangen-Niirnberg, 1970. 8 B. Forster, D. Ropohl and P. Raule, Eine neue Formel zur Beurteilung der Totenstarre: Die Feststellung des FRR-Index. 2. Rechtsmed., 80 (1977) 51-54. 9 G. Beier, E. Liebhardt, M. Schuck and W. Spann, Totenstarremessungen an menschlichen Skelettmuskeln in situ. 2. Rechtsmed., 79 (1977) 277-283. 10 M. Schuck, G. Beier, E. Liebhardt and W. Spann, Zur Schiitzung der Liegezeit durch Messungen der Totenstarre. Beitr. Gerichtl. Med., 36 (1978) 339.-343. 11 T. Krompecher and 0. Frye, Experimental evaluation of rigor mortis. IV. Change in strength and evolution of rigor mortis in the case of physical exercise preceding death. Forensic Sci. Znt., 12 (1978) 103-107. 12 T. Krompecher, Experimental evaluation of rigor mortis. V. Effect of various temperatures on the evolution of rigor mortis. Forensic Sci. Znt., 17 (1981) 19-26. 13 T. Krompecher and 0. Frye, Experimentelle Untersuchungen an der Leichenstarre. II. Das Entstehen der Leichenstarre unter Einfluss von korperlicher Anstrengung. Beitr. Gerichtl. Med., 36 (1978) 345-349. 14 T. Krompecher and 0. Frye, Experimental evaluation of rigor mortis. III. Comparative study of the evolution of rigor mortis in different sized muscle groups in rats. Forensic Sci. Znt., 12 (1978) 97-102. 15 T. Krompecher and 0. Frye, Zur Frage der Todeszeitbestimmung aufgrund der Leichenstarre. Beitr. Gerichtl. Med., 37 (1979) 285-289.