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Diagnostic significance of myofibrillar degeneration of cardiocytes in forensic pathology
Forensic Science Inter-notional, 48 11990) 163- 173 Elsevier Scientific Publishers Ireland Ltd.
163
DIAGNOSTIC SIGNIFICANCE OF MYOFIBRILLAR DEGENERATION OF CARDIOCYTES IN FORENSIC PATHOLOGY*
M. OEHMICHEN, With the technical
I. PEDALb and P. HOHMANN” assistance of A. MERTENa
“Institute of Forensic Medicine at the University of LCbeck, Liibeck Medicine at the University of Heidelberg, Heidelberg IF.R.G.1 (Received June 24th, 19901 (Revision received September (Accepted
September
and “Znstitute of Forensic
4th, 1990)
5th, 19901
Summary The incidence of myofibrillar degeneration (MFD) was studied in the following ensic-pathological diagnostic groups of 25 cases each: acute morphine intoxication, monoxide intoxication, hanging, strangulation by hand/ligature, drowning, acute shock, lethal acute brain injury, explainable death of babies or infants and sudden
different foracute carbon hemorrhagic infant death
syndrome, together with 18 cases of intoxication with various drugs. The MFD was demonstrated by the Luxol-fast-blue reaction, with two types of phenomena being differentiated, namely cross-band lesions and diffuse staining. All diagnostic groups included cases of MFD of differing degrees. Cross-band lesions were observed in practically all cases of hanging, strangulation and acute hemorrhagic shock. Diffuse stain was noted particularly acute brain injury. The diagnostic significance is discussed.
in cases of drowning and
Key words: Myofibrillar degeneration of the cardioeytes; Asphyxia; shock: Brain injury: Intoxication; Sudden infant death syndrome
Drowning;
Hemorrhagic
Introduction Myofibrillar degeneration (MFDl is a myocardial alteration which has been known for decades [lit. see 251 as “hyaline bands” [6, 141,“contraction bands” [28], “coagulative myocytolysis” [4] or “contraction band necrosis” [7]. This alteration has been described particularly with reference to hypoxic myocardial changes [14], but has also occurred with sudden, unexpected cardiac death - in some cases as the only morphological change [1,5,27,30]. Disseminated MFD has also been observed in a number of cases in which the common feature was a final release of catecholamines @it. see 21. It is Address all correspondence and reprint requests to: Prof. Dr. M. Oehmichen, Institut Rechtsmedizin, der Universitat zu Lilbeck, Kahlhorststr. 31-35, D-2400 Lilbeck, F.R.G. *Dedicated to Professor
U. Heifer on the occasion of his 60th birthday.
0379-0738/90/$03.50 0 1990 Elsevier Scientific Publishers Printed and Published in Ireland
Ireland Ltd.
fur
164
generally thought today that catecholamines cause membrane damage which in turn results in an intracytoplasmic calcium increase. The MFD phenomenon as a consequence of catecholamine release is particularly interesting as it is demonstrable within a few minutes of the onset of noxa. According to Reichenbach and Benditt [26] and Arnold [2], MFD is recognizable within 25 min with a peak at 6-8 h and initial signs of clearing after 12 h. Whereas numerous studies of this phenomenon have been carried out on clinicopathological autopsy and biopsy material, almost no systematic investigations have been performed to date in forensic-pathological autopsy material. An overview is available from the year 1980 [9] in which 15 cases of death of different kinds are described; MFD has been described in conjunction with carbon monoxide intoxication [10,19] and drowning [16,20] in animal experiments, cocaine intoxication in humans [29] and isolated cases of sudden infant death syndrome [18]. Excessive MFD has been mentioned in the case of brain damage of different origins [8,11-13,151 and the incidence of MFD has also been associated with shock (hemorrhagic shock [21’23], septic and cardiac shock [2]1and following resuscitation [2,17]. This study was designed to determine the diagnostic significance of MFD in selected forensic-pathological case material and to correlate the different death processes to the occurrence of MFD. Initial findings have already been published in the form of a pilot study [24]. Materials and methods Case material
The selection of case material was based not only on the results of investigations and previous history, but also on the results of the macroscopic, microscopic and toxicological analyses carried out in all cases. The intention was to exclude all influences which might have had an additional bearing on the agony phase. Cases with signs of incipient putrefaction and those in which resuscitation had been attempted were also excluded. The following diagnostic groups were examined: (1) Acute
morphine
intoxication
fn = 25)
Only cases of peracute morphine intoxication on its own were included. Cases with supplementary organic disease, particularly infection, were excluded. These cases were compared with a group of mixed intoxication (n = 61 in which other active ingredients besides morphine were found in toxic concentrations. (21 Carbon monoxide
intoxication
In = 251
Only cases with a carboxyhemoglobin concentration of more than 50% were included, additional cyanide intoxication being excluded. In this way it was possible to eliminate all cases of coronary heart disease or other organic illness in which anoxia might have been the cause of death.
165 TABLE
1
DEMONSTRATION OF MYOFIBRILLARY DEGENERATION WAS CAUSED BY AN ACUTE DRUG INTOXICATION
Dmgs Barbiturates Barbiturates
N
+
12 1
Benzodiazepins Methaqualone Diphenylhydramine Methadone
1 2 1
Ethanol
1
Sum
18
Cross-band lesion ICBL)
IN CASES
Diffuse blue staining IDBSI
9
WHOSE
DEATH
DBL + DBS 3 1
1 1
1 1
10
2
5
(3) Drug intoxication fn = 18) This group included all cases of death through drug intoxication of different types. There were some cases of mixed intoxication, although all cases involving morphine or cocaine were excluded. All detected drugs acted on the CNS (cf. Table 1). 64)Hanging In = 25) This group comprised typical cases and atypical
cases where death resulted from “hanging”, both ones in which no venous congestion was present.
151Strangulation by hand/ligature (n = 25) This group included all cases of strangulation, be it by hand or by ligature. Cases with relevant additional injuries were excluded. (6) Drowning (n = 25) This group included all cases of acute drowning with typical morphology. Cases of reflex death were excluded as were those of indirect drowning, which were recorded separately (n = 4). (7) Acute hemorrhagic shock ln = 25) This group only included cases of peracute loss of blood through stab, cut or shot wounds or spontaneous rupture of a major vessel with morphological indication of exsanguination. (8) Acute brain injury ln = 25) This group included all cases of immediate death, i.e. in less than 45 min, as a result of acute brain injury (Table 2). Cases with a significant loss of
166 TABLE 2 DEMONSTRATION OF A MYOFIBRILLARY DEGENERATION WAS CAUSED BY AN ACUTE BRAIN INJURY
IN CASES WHOSE DEATH
Brain injury
N
Cross-band lesion lCBLl
Gunshot wounds to the brain Impact injury to the brain Stab wounds of the brain stem
11
1
5
4
13
1
6
2
Sum
25
blood were excluded.
Diffuse blue staining (DBSI
1
not taken
DBL DBS
+
1
2
into
12
account.
Cases
with
6
air embolism
were
also
191Sudden infant death syndrome ln = 25) This group exclusively comprised babies of less than 1 year; the diagnosis of sudden infant death syndrome was established after other morphological or toxicological causes of death had been ruled out. TABLE 3 DEMONSTRATION OF MYOFIBRILLARY DEGENERATION OF AN ACUTE, EXPLAINABLE CAUSE OF DEATH Cause of death
Carbon monoxide intoxication Drug intoxication Drowning Strangulation Aspiration Polytrauma Brain injury Perforation of the stomach Starvation Malformation of the heart Hirschsprung’s disease Pneumonia Sum
N
7
IN INFANTS AND CHILDREN
Cross-band lesion ICBLI
Diffuse blue staining
1
2
2
1 2
1 1 1 1
IDBSI
DBL DBS
1 1 2
1 1 1
1 2 25
2 2
6
10
-I
16’7
Fig. 1. Different types of myofibrillar degeneration of cardiocytes. . (a) cross-band lesions after hanging (b) diffuse type of MFD after drowning (a + b: Luxol-fast-blue; a x 500, b x 300).
168
(10) Infants and children
with explainable acute cause of death fn = 25) This group included children who had died acutely as a result of different, definable causes (cf. Table 3). In only three cases were the children older than 1 year (16,22 and 23 months). Histological
preparation
Several blocks of tissue taken from the heart, especially from the left ventricle of each subject were embedded in paraffin after formaldehyde fixation; slices of 5 pm were prepared and stained with Luxol-fast-blue as described by Arnold et al. [3] Evaluation
In the evaluation the incidence of cross-band lesions (Fig. la) and diffuse staining of myocytes (Fig. lb) were recorded separately. The expression of more than 3 fibers with positive reaction per microscopic field was considered as positive. Results
The results for each of the diagnostic groups were shown synoptically (Fig. 21, with only the “drug intoxication” and ‘explainable infant death‘ groups being treated separately (Tables 1 and 31. The following additional annotations should be made: Lfb staining was absent in a total of 22Olo of cases (Fig. 2a) and in about half the cases of morphine and CO intoxication, acute brain injury and sudden infant death syndrome. By contrast, MFD was detected in almost all cases of drug intoxication, hanging, strangulation and acute hemorrhagic shock. Lfb-positive myocytes appeared in disseminated foci, but both types of MFD were distinctly evident in the subendocardial layer of the myocardium. The investigations of several samples per case gave qualitatively identical results per case while quantitative differences could be registered, which are neglected in the course of the present investigation. Cross-band lesions (Fig. 2bl were rare or completely absent in the morphine intoxication, drowning, acute brain injury, sudden infant death syndrome and explained infant death groups. Nearly all Lfb-positive cases in the hanging, strangulation and acute hemorrhagic shock groups were of the cross-band type, generally without additional indication of diffusely stained fibers. Diffuse staining (Fig. 2~) was found without additional crossband lesions in all cases of drowning in which MFD was evident and in more than half the cases of acute brain injury. This phenomenon also occurred in all other groups with the exception of hanging. The percentage of cases with cross-band lesions and diffuse staining
BAND
LESION
Lfb-STAINING
OF MYOCYTES
OF A POSITIVE
BLUE
STAINING
OF MYOCYTES
d)
J_____--
+____
- --i---
CROSS-BAND-LESION+DIFFUSE-BLUE-STAINING
DIFFUSE
Fig. 2. Incidence of positive Luxol-fast-blue (Lfbl staining of cardiocytes including cross-band lesions, diffuse blue staining and cases of both types of lesions simultaneously in different forensic diagnostic groups. Figures as percentage of total number of cases per diagnostic group.
CROSS
INCIDENCE
H
0
0
60
40
20
60
40
20
d)
Fig. 3. Reaction type 1: Summary of diagnostic groups in which cardiocytes tive cases (CBL = cross-band lesion; DBS = diffuse blue staining).
b)
of the cross-band
1
/
type predominate.
Figures
as percentage
of Lfb-posi-
-~ -.--____--.SDS (N=25)
HEMORRHAGIC SHOCK (N=25) mxn1~Oftowmecase.8
p”cm,apa01 tomi me cam.
0.I
a0
60
0
100
100
STRANGLING (N-25)
cl
20
20
a)
40
40
CBL*DBS
60
60
DES
a0
80
CBL only
100
100
HANGING (N-25) arcmt~altot*,mecase*
20
40
60
60
CBL only
1 CBL*oBs
Jm Ilo ncmn
_
of_-_. MIMI ma UM. __
_.___~~__
--
CARBON MONOXIDE INTOX. (N=25) mnwp me a~* ___.__ 01tom ___.-.__.-~-.-
d)
0:
PI IEMW _.__
1
Fig. 4. Reaction type 2 (a,b): Summary of diagnostic groups in which cardiocytes of the diffuse type predominate, . Reaction type 3 k,d): Summary of diagnostic groups containing cross-band lesions, diffuse staining, a combination of both and no staining. Figures as percentage of Lfb-positive cases (CBL = cross-band lesion; DBS = diffuse blue staining).
b)
-
ACUTE BFVUN INJURY (N925) p.rcmntag. 01total Ill. U”. ,ooy-__ _.______._______~.---
a
~_.__
20
20
---
40
40
__
60
60
0
60
100
ACUTE MORPHIN INTOXICATION (N-25)
60
100
DROWNING (N=25) wcmtag. ottotal HI* __.___.____ __.ca”. - -
172 together (Fig. 2d) was relatively acute brain injury and explained
high in the intoxication infant death (Table 31.
groups, cases with
Discussion
The study showed Lfb-positive cardiocyte staining in the majority of cases examined (197 out of 253 = 78%). As MFD can occur in a variety of illnesses and injuries, this observation confirms the findings of other studies but does not allow any further diagnostic conclusions to be drawn as such from the case material selected here. In order to establish whether this phenomenon is so common as to be demonstrable in all cases, an attempt was made to isolate a group without incidence of MFD. No completely negative group could be found, although the morphine and CO intoxication groups showed comparatively fewer cases of Lfb staining. Despite this limitation, reaction types may be distinguished which could be helpful in differential diagnosis: Reaction type 1: cross-band lesions - observed in the hanging, strangulation, acute hemorrhagic shock and sudden infant death syndrome groups (Fig. 3). Reaction type 2: diffuse staining - observed in the drowning and acute brain injury groups (Figs. 4a,b). Reaction type 3: combined incidence of cross-band lesions and diffuse staining - observed in the morphine and CO intoxication groups (Fig. 4c,dl. With regard to the cases of explainable death of infants and small chiG dren it appears that the course of death might be influenced by additional factors, as the cross-band lesion and diffuse staining phenomena were distributed somewhat differently than in the adult cases. It was also noted that the cross-band lesion phenomenon occurred rarely in the peracute brain injury group, an observation which conflicts with the findings of previous studies. A possible explanation might be the different survival periods: in our cases the maximum survival period was 45 min, whereas the quoted cases feature survival periods of hours or days. The role of the time factor in diffuse staining and cross-band lesions might also be questioned. References L.C. Armiger and W.M.I. Smeeton, Contraction-band necrosis: patterns of distribution in the myocardium and their diagnostic usefulness in sudden cardiac death. Pathology, 18 (19861289 - 295. G. Arnold, Myofibrilldire Degeneration des Myokards. Phdinomenologie, Vorkommen und Pathogenese. Habilschrift, Kiiln, (19861. G. Arnold, C. Kaiser and R. Fischer, Myofibrillary degeneration - a common type of myocardial lesion and its selective identification by a modified 1~x01 fast blue stain. Path01 Res. Pm&., 180 (19851405-415. G. Baroldi, Different types of myocardial necrosis in coronary heart disease: A pathophysiologic of their functional significance. Am. Heart. J., 89 (19751742 - 752.
173 5 6
7
a 9
10 11 12 13 14 15
16 17
G. Baroldi, G. Falzi and F. Mariani, Significance of morphological changes in sudden coronary death. Adv. CardioL, 25 (1978182-95. F. Biichner and W.v.Luxadou, Elektrokardiographische Veranderungen und disseminierte Nekrosen des Herzmuskels bei experimenteller Koronarinsuffizienz. Be&. PathoL Anut., 93 (1934) 169- 197. B.H. Bulkley, R.L. Ridolfi, W.R. Salyer and G.M. Hutchins, Myocardial lesions of progressive systemic sclerosis. A cause of cardiac dysfunction. Circulation, 53 (19761483- 490. G.E. Burch, S.C. Sun, H.L. Colcolough, N.P. DePasquale and R.S. Sohal, Acute myocardial lesions. Arch. PathoL, 84 (19671 517-521. M.S. Cebelin and C.S. Hirsch, Human stress cardiomyopathy. Myocardial lesions in victims of homicidal assaults without internal injuries. Hum. PathoL, 11 (19801 123- 132. C. Christ, Experimentelle Kohlenoxydvergiftung. Herzmuskelnekrosen und Elektrokardiogramm. Be&. PathoL Anut., 94 (19341 111- 125. R.C.R. Connor, Heart damage associated with intracranial lesions. Br. Med. J., 3 (1968) 2931. R.C.R. Connor, Myocardial damage secondary to brain lesions. Am. Heart J., 78 (19691 145148. J.H. Greenhoot and D.D. Reiehenbach, Cardiac injury and subarachnoid hemorrhage. J. Neusosurg., 30 (1969) 521- 531. E. Grundmann, Histologische Untersuchungen ilber die Wirkungen experimentellen Sauerstoffmangels auf das Katzenherz. Be&. Anut., 111 (1950151136-76. K.E. Hammermeister and D.D. Reichenbach, QRS-changes pulmonary edema and myocardial necrosis associated with subarachnoid hemorrhage. Am. Heart J., 78 (1969194100. S.B. Karch, Pathology of the heart in drowning. Arch. PathoL, 109 (1985) 176- 178. S.B. Karch, Resuscitation-induced myocardial necrosis. Am. J. Forensic Med. PathoL, (1987) 3-8.
18 19
20 21 22 23 24
25 26 27 28
29
30
J. Kariks, Cardiac lesions in sudden infant death syndrome. Forensic Sci Znt., 39 (1988) 211 -225. K. Kjeldsen, H.K. Thomsen and P. Astrup, Effect of carbon monoxide on myocardium: Ultrastructural changes in rabbits after moderate, chronic exposure. Circ. Res., 34 (19741 339 - 348. D.W.R. Lunt and A.G.Rose, Pathology of the human heart in drowning. Awh. PathoL Lab. Me&, 111 (19871939-942. A.M. Martin and D.B. Hackel. The myocardium of the dog in hemorrhagic shock. Lab. Invest., 12 (1963) 77-91. A.M. Martin and D.B. Hackel, An electron microscopic study of the progression of myocardial lesions in the dog after hemorrhagic shock. Lab. Invest., 15 (19661243-260. A.M. Martin, D.B. Hackel and S.M. Kurtz, The ultrastructure of zonal lesions of the myocardium in hemorrhagic shock. Am. J. PathoL, 44 (1964) 127-140. M. Oehmichen, I. Pedal and P. Hohmann, Myofibrillare Degeneration der Herzmuskulatur: Diagnostische Wertigkeit am ausgesuchten forensisch-pathologischen Fallmaterial. Be&. GetihtL Med., 48 (19901245-249. I. Pedal and M. Oehmichen. MyofibrillPre Degeneration der Herzmuskulatur: Histologisches Bild und pathophysiologische Deutung. Be&. Gerichtl Med, 48 (19901237 - 244. D.D. Reichenbach and E.P. Benditt. Catecholamines and cardiomyopathy: The pathogenesis and potential importance of myofibrillar degeneration. Hum. PathoL, 1 (1970) 125- 150. D.D. Reichenbach and N.S. Moss, Myocardial cell necrosis and sudden death in humans. Circulation 52 Suppl., III, (1975160-62. H.M. Sommers and R.B. Jennings, Experimental acute myoeardial infarction. Histologic and histochemical studies of early myocardial infarcts induced by temporary or permanent occlusion of a coronary artery. Lab. Invest., 13 (1964) 1491- 1503. H.O. Tazelaar, S.B. Karch, B.G. Stephens and M.E. Billingsham, Cocaine and the heart. Hum. PathoL, 18 (19871 195- 199. G. Thiene, A. Nava, D. Corrado, L. Rossi and N. Pennelli, Right ventricular cardiomyopathy and sudden death in young people. N, EngL J. Med., 318 (19881129- 133.
163
DIAGNOSTIC SIGNIFICANCE OF MYOFIBRILLAR DEGENERATION OF CARDIOCYTES IN FORENSIC PATHOLOGY*
M. OEHMICHEN, With the technical
I. PEDALb and P. HOHMANN” assistance of A. MERTENa
“Institute of Forensic Medicine at the University of LCbeck, Liibeck Medicine at the University of Heidelberg, Heidelberg IF.R.G.1 (Received June 24th, 19901 (Revision received September (Accepted
September
and “Znstitute of Forensic
4th, 1990)
5th, 19901
Summary The incidence of myofibrillar degeneration (MFD) was studied in the following ensic-pathological diagnostic groups of 25 cases each: acute morphine intoxication, monoxide intoxication, hanging, strangulation by hand/ligature, drowning, acute shock, lethal acute brain injury, explainable death of babies or infants and sudden
different foracute carbon hemorrhagic infant death
syndrome, together with 18 cases of intoxication with various drugs. The MFD was demonstrated by the Luxol-fast-blue reaction, with two types of phenomena being differentiated, namely cross-band lesions and diffuse staining. All diagnostic groups included cases of MFD of differing degrees. Cross-band lesions were observed in practically all cases of hanging, strangulation and acute hemorrhagic shock. Diffuse stain was noted particularly acute brain injury. The diagnostic significance is discussed.
in cases of drowning and
Key words: Myofibrillar degeneration of the cardioeytes; Asphyxia; shock: Brain injury: Intoxication; Sudden infant death syndrome
Drowning;
Hemorrhagic
Introduction Myofibrillar degeneration (MFDl is a myocardial alteration which has been known for decades [lit. see 251 as “hyaline bands” [6, 141,“contraction bands” [28], “coagulative myocytolysis” [4] or “contraction band necrosis” [7]. This alteration has been described particularly with reference to hypoxic myocardial changes [14], but has also occurred with sudden, unexpected cardiac death - in some cases as the only morphological change [1,5,27,30]. Disseminated MFD has also been observed in a number of cases in which the common feature was a final release of catecholamines @it. see 21. It is Address all correspondence and reprint requests to: Prof. Dr. M. Oehmichen, Institut Rechtsmedizin, der Universitat zu Lilbeck, Kahlhorststr. 31-35, D-2400 Lilbeck, F.R.G. *Dedicated to Professor
U. Heifer on the occasion of his 60th birthday.
0379-0738/90/$03.50 0 1990 Elsevier Scientific Publishers Printed and Published in Ireland
Ireland Ltd.
fur
164
generally thought today that catecholamines cause membrane damage which in turn results in an intracytoplasmic calcium increase. The MFD phenomenon as a consequence of catecholamine release is particularly interesting as it is demonstrable within a few minutes of the onset of noxa. According to Reichenbach and Benditt [26] and Arnold [2], MFD is recognizable within 25 min with a peak at 6-8 h and initial signs of clearing after 12 h. Whereas numerous studies of this phenomenon have been carried out on clinicopathological autopsy and biopsy material, almost no systematic investigations have been performed to date in forensic-pathological autopsy material. An overview is available from the year 1980 [9] in which 15 cases of death of different kinds are described; MFD has been described in conjunction with carbon monoxide intoxication [10,19] and drowning [16,20] in animal experiments, cocaine intoxication in humans [29] and isolated cases of sudden infant death syndrome [18]. Excessive MFD has been mentioned in the case of brain damage of different origins [8,11-13,151 and the incidence of MFD has also been associated with shock (hemorrhagic shock [21’23], septic and cardiac shock [2]1and following resuscitation [2,17]. This study was designed to determine the diagnostic significance of MFD in selected forensic-pathological case material and to correlate the different death processes to the occurrence of MFD. Initial findings have already been published in the form of a pilot study [24]. Materials and methods Case material
The selection of case material was based not only on the results of investigations and previous history, but also on the results of the macroscopic, microscopic and toxicological analyses carried out in all cases. The intention was to exclude all influences which might have had an additional bearing on the agony phase. Cases with signs of incipient putrefaction and those in which resuscitation had been attempted were also excluded. The following diagnostic groups were examined: (1) Acute
morphine
intoxication
fn = 25)
Only cases of peracute morphine intoxication on its own were included. Cases with supplementary organic disease, particularly infection, were excluded. These cases were compared with a group of mixed intoxication (n = 61 in which other active ingredients besides morphine were found in toxic concentrations. (21 Carbon monoxide
intoxication
In = 251
Only cases with a carboxyhemoglobin concentration of more than 50% were included, additional cyanide intoxication being excluded. In this way it was possible to eliminate all cases of coronary heart disease or other organic illness in which anoxia might have been the cause of death.
165 TABLE
1
DEMONSTRATION OF MYOFIBRILLARY DEGENERATION WAS CAUSED BY AN ACUTE DRUG INTOXICATION
Dmgs Barbiturates Barbiturates
N
+
12 1
Benzodiazepins Methaqualone Diphenylhydramine Methadone
1 2 1
Ethanol
1
Sum
18
Cross-band lesion ICBL)
IN CASES
Diffuse blue staining IDBSI
9
WHOSE
DEATH
DBL + DBS 3 1
1 1
1 1
10
2
5
(3) Drug intoxication fn = 18) This group included all cases of death through drug intoxication of different types. There were some cases of mixed intoxication, although all cases involving morphine or cocaine were excluded. All detected drugs acted on the CNS (cf. Table 1). 64)Hanging In = 25) This group comprised typical cases and atypical
cases where death resulted from “hanging”, both ones in which no venous congestion was present.
151Strangulation by hand/ligature (n = 25) This group included all cases of strangulation, be it by hand or by ligature. Cases with relevant additional injuries were excluded. (6) Drowning (n = 25) This group included all cases of acute drowning with typical morphology. Cases of reflex death were excluded as were those of indirect drowning, which were recorded separately (n = 4). (7) Acute hemorrhagic shock ln = 25) This group only included cases of peracute loss of blood through stab, cut or shot wounds or spontaneous rupture of a major vessel with morphological indication of exsanguination. (8) Acute brain injury ln = 25) This group included all cases of immediate death, i.e. in less than 45 min, as a result of acute brain injury (Table 2). Cases with a significant loss of
166 TABLE 2 DEMONSTRATION OF A MYOFIBRILLARY DEGENERATION WAS CAUSED BY AN ACUTE BRAIN INJURY
IN CASES WHOSE DEATH
Brain injury
N
Cross-band lesion lCBLl
Gunshot wounds to the brain Impact injury to the brain Stab wounds of the brain stem
11
1
5
4
13
1
6
2
Sum
25
blood were excluded.
Diffuse blue staining (DBSI
1
not taken
DBL DBS
+
1
2
into
12
account.
Cases
with
6
air embolism
were
also
191Sudden infant death syndrome ln = 25) This group exclusively comprised babies of less than 1 year; the diagnosis of sudden infant death syndrome was established after other morphological or toxicological causes of death had been ruled out. TABLE 3 DEMONSTRATION OF MYOFIBRILLARY DEGENERATION OF AN ACUTE, EXPLAINABLE CAUSE OF DEATH Cause of death
Carbon monoxide intoxication Drug intoxication Drowning Strangulation Aspiration Polytrauma Brain injury Perforation of the stomach Starvation Malformation of the heart Hirschsprung’s disease Pneumonia Sum
N
7
IN INFANTS AND CHILDREN
Cross-band lesion ICBLI
Diffuse blue staining
1
2
2
1 2
1 1 1 1
IDBSI
DBL DBS
1 1 2
1 1 1
1 2 25
2 2
6
10
-I
16’7
Fig. 1. Different types of myofibrillar degeneration of cardiocytes. . (a) cross-band lesions after hanging (b) diffuse type of MFD after drowning (a + b: Luxol-fast-blue; a x 500, b x 300).
168
(10) Infants and children
with explainable acute cause of death fn = 25) This group included children who had died acutely as a result of different, definable causes (cf. Table 3). In only three cases were the children older than 1 year (16,22 and 23 months). Histological
preparation
Several blocks of tissue taken from the heart, especially from the left ventricle of each subject were embedded in paraffin after formaldehyde fixation; slices of 5 pm were prepared and stained with Luxol-fast-blue as described by Arnold et al. [3] Evaluation
In the evaluation the incidence of cross-band lesions (Fig. la) and diffuse staining of myocytes (Fig. lb) were recorded separately. The expression of more than 3 fibers with positive reaction per microscopic field was considered as positive. Results
The results for each of the diagnostic groups were shown synoptically (Fig. 21, with only the “drug intoxication” and ‘explainable infant death‘ groups being treated separately (Tables 1 and 31. The following additional annotations should be made: Lfb staining was absent in a total of 22Olo of cases (Fig. 2a) and in about half the cases of morphine and CO intoxication, acute brain injury and sudden infant death syndrome. By contrast, MFD was detected in almost all cases of drug intoxication, hanging, strangulation and acute hemorrhagic shock. Lfb-positive myocytes appeared in disseminated foci, but both types of MFD were distinctly evident in the subendocardial layer of the myocardium. The investigations of several samples per case gave qualitatively identical results per case while quantitative differences could be registered, which are neglected in the course of the present investigation. Cross-band lesions (Fig. 2bl were rare or completely absent in the morphine intoxication, drowning, acute brain injury, sudden infant death syndrome and explained infant death groups. Nearly all Lfb-positive cases in the hanging, strangulation and acute hemorrhagic shock groups were of the cross-band type, generally without additional indication of diffusely stained fibers. Diffuse staining (Fig. 2~) was found without additional crossband lesions in all cases of drowning in which MFD was evident and in more than half the cases of acute brain injury. This phenomenon also occurred in all other groups with the exception of hanging. The percentage of cases with cross-band lesions and diffuse staining
BAND
LESION
Lfb-STAINING
OF MYOCYTES
OF A POSITIVE
BLUE
STAINING
OF MYOCYTES
d)
J_____--
+____
- --i---
CROSS-BAND-LESION+DIFFUSE-BLUE-STAINING
DIFFUSE
Fig. 2. Incidence of positive Luxol-fast-blue (Lfbl staining of cardiocytes including cross-band lesions, diffuse blue staining and cases of both types of lesions simultaneously in different forensic diagnostic groups. Figures as percentage of total number of cases per diagnostic group.
CROSS
INCIDENCE
H
0
0
60
40
20
60
40
20
d)
Fig. 3. Reaction type 1: Summary of diagnostic groups in which cardiocytes tive cases (CBL = cross-band lesion; DBS = diffuse blue staining).
b)
of the cross-band
1
/
type predominate.
Figures
as percentage
of Lfb-posi-
-~ -.--____--.SDS (N=25)
HEMORRHAGIC SHOCK (N=25) mxn1~Oftowmecase.8
p”cm,apa01 tomi me cam.
0.I
a0
60
0
100
100
STRANGLING (N-25)
cl
20
20
a)
40
40
CBL*DBS
60
60
DES
a0
80
CBL only
100
100
HANGING (N-25) arcmt~altot*,mecase*
20
40
60
60
CBL only
1 CBL*oBs
Jm Ilo ncmn
_
of_-_. MIMI ma UM. __
_.___~~__
--
CARBON MONOXIDE INTOX. (N=25) mnwp me a~* ___.__ 01tom ___.-.__.-~-.-
d)
0:
PI IEMW _.__
1
Fig. 4. Reaction type 2 (a,b): Summary of diagnostic groups in which cardiocytes of the diffuse type predominate, . Reaction type 3 k,d): Summary of diagnostic groups containing cross-band lesions, diffuse staining, a combination of both and no staining. Figures as percentage of Lfb-positive cases (CBL = cross-band lesion; DBS = diffuse blue staining).
b)
-
ACUTE BFVUN INJURY (N925) p.rcmntag. 01total Ill. U”. ,ooy-__ _.______._______~.---
a
~_.__
20
20
---
40
40
__
60
60
0
60
100
ACUTE MORPHIN INTOXICATION (N-25)
60
100
DROWNING (N=25) wcmtag. ottotal HI* __.___.____ __.ca”. - -
172 together (Fig. 2d) was relatively acute brain injury and explained
high in the intoxication infant death (Table 31.
groups, cases with
Discussion
The study showed Lfb-positive cardiocyte staining in the majority of cases examined (197 out of 253 = 78%). As MFD can occur in a variety of illnesses and injuries, this observation confirms the findings of other studies but does not allow any further diagnostic conclusions to be drawn as such from the case material selected here. In order to establish whether this phenomenon is so common as to be demonstrable in all cases, an attempt was made to isolate a group without incidence of MFD. No completely negative group could be found, although the morphine and CO intoxication groups showed comparatively fewer cases of Lfb staining. Despite this limitation, reaction types may be distinguished which could be helpful in differential diagnosis: Reaction type 1: cross-band lesions - observed in the hanging, strangulation, acute hemorrhagic shock and sudden infant death syndrome groups (Fig. 3). Reaction type 2: diffuse staining - observed in the drowning and acute brain injury groups (Figs. 4a,b). Reaction type 3: combined incidence of cross-band lesions and diffuse staining - observed in the morphine and CO intoxication groups (Fig. 4c,dl. With regard to the cases of explainable death of infants and small chiG dren it appears that the course of death might be influenced by additional factors, as the cross-band lesion and diffuse staining phenomena were distributed somewhat differently than in the adult cases. It was also noted that the cross-band lesion phenomenon occurred rarely in the peracute brain injury group, an observation which conflicts with the findings of previous studies. A possible explanation might be the different survival periods: in our cases the maximum survival period was 45 min, whereas the quoted cases feature survival periods of hours or days. The role of the time factor in diffuse staining and cross-band lesions might also be questioned. References L.C. Armiger and W.M.I. Smeeton, Contraction-band necrosis: patterns of distribution in the myocardium and their diagnostic usefulness in sudden cardiac death. Pathology, 18 (19861289 - 295. G. Arnold, Myofibrilldire Degeneration des Myokards. Phdinomenologie, Vorkommen und Pathogenese. Habilschrift, Kiiln, (19861. G. Arnold, C. Kaiser and R. Fischer, Myofibrillary degeneration - a common type of myocardial lesion and its selective identification by a modified 1~x01 fast blue stain. Path01 Res. Pm&., 180 (19851405-415. G. Baroldi, Different types of myocardial necrosis in coronary heart disease: A pathophysiologic of their functional significance. Am. Heart. J., 89 (19751742 - 752.
173 5 6
7
a 9
10 11 12 13 14 15
16 17
G. Baroldi, G. Falzi and F. Mariani, Significance of morphological changes in sudden coronary death. Adv. CardioL, 25 (1978182-95. F. Biichner and W.v.Luxadou, Elektrokardiographische Veranderungen und disseminierte Nekrosen des Herzmuskels bei experimenteller Koronarinsuffizienz. Be&. PathoL Anut., 93 (1934) 169- 197. B.H. Bulkley, R.L. Ridolfi, W.R. Salyer and G.M. Hutchins, Myocardial lesions of progressive systemic sclerosis. A cause of cardiac dysfunction. Circulation, 53 (19761483- 490. G.E. Burch, S.C. Sun, H.L. Colcolough, N.P. DePasquale and R.S. Sohal, Acute myocardial lesions. Arch. PathoL, 84 (19671 517-521. M.S. Cebelin and C.S. Hirsch, Human stress cardiomyopathy. Myocardial lesions in victims of homicidal assaults without internal injuries. Hum. PathoL, 11 (19801 123- 132. C. Christ, Experimentelle Kohlenoxydvergiftung. Herzmuskelnekrosen und Elektrokardiogramm. Be&. PathoL Anut., 94 (19341 111- 125. R.C.R. Connor, Heart damage associated with intracranial lesions. Br. Med. J., 3 (1968) 2931. R.C.R. Connor, Myocardial damage secondary to brain lesions. Am. Heart J., 78 (19691 145148. J.H. Greenhoot and D.D. Reiehenbach, Cardiac injury and subarachnoid hemorrhage. J. Neusosurg., 30 (1969) 521- 531. E. Grundmann, Histologische Untersuchungen ilber die Wirkungen experimentellen Sauerstoffmangels auf das Katzenherz. Be&. Anut., 111 (1950151136-76. K.E. Hammermeister and D.D. Reichenbach, QRS-changes pulmonary edema and myocardial necrosis associated with subarachnoid hemorrhage. Am. Heart J., 78 (1969194100. S.B. Karch, Pathology of the heart in drowning. Arch. PathoL, 109 (1985) 176- 178. S.B. Karch, Resuscitation-induced myocardial necrosis. Am. J. Forensic Med. PathoL, (1987) 3-8.
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25 26 27 28
29
30
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