PATHOLOGICAL CHANGES IN THE LIVER AND LUNGS IN STRANGULATION MECHANICAL ASPHYXIA

Аннотация

Strangulation is one of the classical forms of mechanical asphyxia that results from external compression of the neck, leading to hypoxia and, ultimately, death. While most forensic investigations of strangulation focus on cervical structures, this article investigates the secondary pathological changes observed in the liver and lungs as a result of systemic hypoxia, venous stasis, and circulatory arrest. Particular emphasis is placed on postmortem findings, histopathological alterations, and the medico-legal value of these changes in diagnosing the cause and mechanism of death. The article provides an in-depth review of tissue morphology, congestion patterns, hepatocellular and alveolar responses, and the forensic implications of such findings in both typical and atypical asphyxial deaths. Kеywоrds: Strangulation, mechanical asphyxia, pathological anatomy, lung congestion, hepatic hypoxia, postmortem examination, venous stasis, forensic pathology, asphyxial death, histopathology. INTRОDUСTIОN Mechanical asphyxia resulting from strangulation represents a critical area of forensic pathology, particularly in criminal cases involving homicidal violence. Strangulation may be manual (throttling), ligature-based, or hanging-related, but in all cases, external force obstructs the airways and/or cervical blood vessels, culminating in cerebral anoxia. While much attention is directed toward cervical and facial findings—such as petechial hemorrhages, ecchymoses, hyoid bone fractures—the systemic consequences of asphyxia often extend beyond the neck region, inducing widespread alterations in internal organs due to oxygen deprivation and impaired circulation. The liver and lungs, as highly vascularized and metabolically active organs, are among the most sensitive to hypoxic injury. In cases of strangulation, the immediate consequence is a combination of venous congestion, hypostatic blood pooling, and progressive cellular degeneration. These changes, although not always pathognomonic, can provide crucial corroborative evidence supporting the diagnosis of asphyxial death, especially when neck findings are equivocal orabsent. Therefore, understanding the pathological transformations in these organs enhances the forensic pathologist’s ability to reconstruct the antemortem events and differentiate between vital and postmortem phenomena [1]. MАTЕRIАLSАNDMЕTHОDS The lungs, as the primary organs of gas exchange, are directly affected by the cessation of respiration and venous return associated with strangulation. Macroscopically, lungs in such cases are typically overinflated, heavy, and exhibit a dark-purple coloration due to intense hypostatic congestion and venous stasis. Upon sectioning, the parenchyma exudes a dark, frothy, blood- tinged fluid—afinding known as “asphyxial edema.” www.wordlyknowledge.uz ILMIYMETODIK JURNAL JOURNAL OFIQRO –ЖУРНАЛ ИҚРО –IQRO JURNALI –volume 15,issue01,2025 ISSN:2181-4341, IMPACT FACTOR( RESEARCH BIB )–7,245,SJIF–5,431 One of the most characteristic microscopic features is alveolar overdistension, often accompanied by interalveolar septal rupture, particularly in individuals who struggled prior to death. Capillary engorgement, interstitial hemorrhages, and perivascular leakage are frequently observed. In some cases, diffuse alveolar damage (DAD) mimicking early acute respiratory distress syndrome (ARDS) may also be noted, especially in prolonged survival following strangulation [2]. Focal emphysematous changes, especially near the periphery of the lungs, reflect the victim’s forceful inspiratory efforts during the terminal phase. These findings, while not specific to strangulation, are consistent with mechanical asphyxia and assist in distinguishing it from natural deaths or sudden cardiac arrests. The presence of widespread petechiae on pleural surfaces, particularly the visceral pleura, further corroborates venous obstruction and is considered a classic hallmark ofasphyxia in general. RЕSULTSАNDDISСUSSIОN The liver, although not in the direct pathway of strangulation trauma, undergoes significant pathophysiological changes secondary to systemic hypoxia, venous congestion, and circulatory standstill. On gross examination, the liver appears enlarged, tense, and dark reddish-brown. The surface may show a “mottled” appearance due to hypostatic pooling and early autolytic changes independent zones [3]. Histologically, the liver demonstrates features of centrilobular (zone III) congestion, which is most pronounced in asphyxial deaths. The central veins and sinusoids are markedly dilated and filled with stagnant blood. Hepatocellular ballooning, vacuolar degeneration, and pyknotic nuclei are observed in hepatocytes deprived of oxygen. These findings reflect early ischemic necrosis, which progresses rapidly in the postmortem period if the death was preceded by prolonged hypoxia. In addition, microthrombi formation in hepatic sinusoids may be seen in prolonged agony or delayed death, indicating a d