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RESULTS
Gross examination of muscle yielded no relevant findings
in any of the groups. Histological changes observed, together FIGURE 1. Drowning group. Soleus muscle. Hypercontracted fibers
with the results of semiquantitative analysis for the 3 groups, (arrows) showed great size, high staining, and rounded profiles.
are shown in Table 1. No structural abnormalities were noted Masson trichrome, original magnification 20.
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FIGURE 2. Drowning group. Anterior tibial muscle. Many very large FIGURE 4. Drowning group. Anterior tibial muscle. Three muscle
fibers showing distortions of their architecture (whorled fibers) fibers showed basophilic granular stain (head arrows) that
(arrows). Hematoxylin-eosin, original magnification 10. corresponds with the ragged red fiber. Hematoxylin-eosin, original
magnification 40.
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FIGURE 5. Drowning group. Sternohyoid muscle. Muscle fibers showing degenerative changes include ghosts or pale fibers (arrows) along
with others containing reddish mass inside. There is also interstitial edema. Masson trichrome, original magnification 40.
with which they appeared suggests that they were formed may well be that in response to the lack of oxygen prompted both
equally fast. by drowning and by hypovolemic shock, muscle mitochondria
Although MGT-detected structural abnormalities were accumulate rapidly in the vicinity of muscle capillaries to enhance
much more marked in the drowning group, they also were the efficacy of their oxidative metabolism, or simply that they
observed—albeit less frequently—in the exsanguination group, undergo an immediate pathological reaction. In normal muscle
suggesting a common or similar mechanism in both types of fibers, subsarcolemmal mitochondria are known to accumulate
death. This may be linked to the marked hypoxemia undergone close to capillaries to optimize the supply of oxygen and sub-
by muscle fibers in both situations: in the drowning group due strates.21,22 Modifications in the capillary network and in muscle
to asphyxia caused by liquid entering the airways, and in the ex- fibers—particularly changes in mitochondrial volume density—
sanguination group to sudden hypovolemic shock. It seems that are known to take place in response to changing functional de-
the intense “hypoxia” underwent by the exsanguination and mands due to hypoxia linked both to extreme altitude23 and
drowning rats gives time for the mitochondrial changes to occur to prolonged submersion.24 Adaptation of this kind, however,
while the group of cervical dislocation does not have enough time. takes place progressively; here, rather than a gradual adaptation,
In any case, these muscle changes, suggestive of intense anoxia, modifications were part of a very fast fiber response to severe
might be seen in other kind of asphyxial deaths and cannot be con- hypoxia. This might lead to the rapid formation of large mito-
sidered as specific of drowning deaths. chondrial clumps and thus to the appearance of ragged red fi-
Although the precise mechanism leading to the formation bers staining abnormally to MGT. This would seem to be
of ragged red fiber and abnormal clumps of red material in the borne out by the mitochondrial response to hypoxia. Muscle
muscles studied here cannot yet be identified beyond doubt, it mitochondria display an early reaction to ischemia; 2 to
FIGURE 6. Drowning group. Anterior tibial muscle. Presence of red staining material with different morphologies in several muscle fibers
is prominent: peripheral balloons (arrowhead), crescent or ridge (thick arrow), and interstitial red material (thin arrows). MGT, original
magnification 40.
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However, we cannot rule out completely the possible role of ago- or disruption of contractile material32,33; forced lengthening con-
nal convulsions as a cause of these degenerative changes, which tractions have been found to induce the formation of swollen,
could also take place in other asphyxial deaths as a consequence rounded fibers due to disruption of the plasma membrane, appar-
of intense muscle spasms. The high levels of myoglobin in urine ent in irregular dystrophin staining.34 It has been suggested that
reported in some causes of death, including drowning, are severe damage to the plasma membrane due to mechanical
regarded as an indicator of muscle hyperactivity.30 Concentric trauma may cause a massive influx of Ca++ and thence to
muscle actions—including swimming and diaphragmatic hypercontraction.35 Ghost-like fibers are nonspecific degenerative
breathing—appear to reproduce the patterns seen in traumatic fibers appearing in a whole range of myopathic disorders, includ-
injuries such as crush or overstrain.31 Strenuous high-intensity ing rhabdomyolysis; the main morphological feature of these early
exercise is known to lead to muscle damage characterized by rupture degenerative fibers is their pallor on histological staining and loss
of activity on histochemical examination.35 These varying degrees
of myofibrillar lesion may therefore be regarded as an expression
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FIGURE 16. Exsanguination group. Diaphragm muscle. Several FIGURE 18. Cervical dislocation group. Diaphragm muscle. Muscle
muscle fibers showing red peripheral balloons. MGT, original fibers do not show abnormalities. MGT, original
magnification 20. magnification 40.
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28. Warren JD, Blumbergs PC, Thompson PD. Rhabdomyolysis: a review. 32. Salminen A, Vihko V. Susceptibility of mouse skeletal muscles to exercise
Muscle Nerve. 2002;25:332–347. injuries. Muscle Nerve. 1983;8:596–601.
29. Seong EY, Rhee H, Lee N, et al. A case of severe acute kidney 33. Magaudda L, Di Mauro D, Trimarchi F, et al. Effects of physical exercise
injury by near-drowning. J Korean Med Sci. 2012;27: on skeletal muscle fiber: ultrastructural and molecular aspects. Basic Appl
218–220. Myol. 2004;14:17–21.
30. Zhu BL, Ishida K, Quan L, et al. Post-mortem urinary myoglobin 34. Komulainen J, Takala TE, Kuipers H, et al. The disruption of myofibre
levels with reference to the causes of death. Forensic Sci Int. structures in rat skeletal muscle after forced lengthening contractions.
2001;115:183–188. Pflugers Arch. 1998;436:735–741.
31. Stauber WT, Smith CA. Cellular responses in exertion-induced 35. Carpenter S, Karpati G. Pathology of Skeletal Muscle. 2nd ed. New York,
skeletal muscle injury. Mol Cell Biochem. 1998;179:189–196. NY: Oxford University Press; 2001.
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