Pathological spectrum of the lung in cases of violent death: Part I. Lesion classification

The results are presented of the pathological study of the lungs in 66 cases of violent death observing the more frequent types of lesions and establishing 4 different groups of postlesioned pulmonary condition. 1. Inflammatory alveolar lesions without a diffused interstitial involvement (IAL) including contusions or direct aggressions, lobular pneumonias, or bronchopneumonias with a predominance of intra-alveolar inflammatory exudation. 2. Inflammatory alveolar lesions with a diffuse interstitial involvement (IALW) including generalized affectation of the parenchyma with lesions in the capillary structure of the wall. 3. Edemohemorrhagic lesions (EHL) presenting phenomena of capillary congestion with hematic extravasation and interstitial and intra-alveolar edema, without inflammatory involvement. This is the most numerous group and it can constitute the preliminary stage of any other. 4. Unspecific chronic lesions (UCL) not related to the cause of death, being chronically inflammatory and fibrotic alterations of limited interest in our study. We emphasize the importance of the inflammatory involvement of the alveolar wall in the pathogenia of diffuse alveolar damage (DAD) and the aggravation of pulmonary lesions by capillary structure alteration, direct lesion of alveolar epithelium, presence of macrophages, and liberation of certain intracellular enzymes.     

Pulmonary edema in fatal heroin overdose: immunohistological investigations with IgE, collagen IV and laminin - no increase of defects of alveolar-capillary membranes

Pulmonary edema complicating heroin overdosage is a well recognized entity and regarded as the major mechanism contributing to death in heroin addicts. It's pathogenesis is unknown, several mechanisms are discussed: hypoxia-induced increase of pulmonary capillary permeability, depressed myocardial contractility, centrally induced respiratory depression, primary toxic effects on the alveolar capillaries and acute anaphylactic shock. The present study included opiate-related deaths (n=23) and a control group of sudden cardiovascular deaths (n=12) to verify the hypothesis, that defects of the alveolar capillary membranes and/or an acute anaphylactic reaction leads to pulmonary congestion, edema and hemorrhages. Lung specimens were obtained from these 35 autopsies of persons autopsied in the Institute of Forensic Medicine, University of Bonn, in 1997 and 1998. All specimens were examined with hematoxylin-eosin, prussian blue and investigated with immunohistological methods using primary antibodies against collagen IV, laminin and IgE. Defects of the basal laminae of the alveoli were found, demonstrated by laminin and collagen IV, and the number of IgE-positive cells was counted in both groups. There was an increased but not significant number of IgE-positive cells in the heroin-group and defects of the epithelial and endothelial basal laminae were found in both groups without significant differences.     

Histomorphologic lung findings in long-term artificial respiration with special reference to extreme continuous artificial respiration using pure oxygen

The respirator lung is characterized histologically in the first exudative phase by capillary congestion, intra-alveolary edema, hyaline membranes and in most cases by concomitant inflammatory alterations. In the following irreversible phase, fibrous organization processes dominate and show a variable tendency towards pulmonary fibrosis. In 27 cases with long-term artificial respiration from 4 days to 12 weeks, mainly the proliferative alterations were investigated. In 18 cases, the histopathological findings indicated fibrosis of the alveolar septa with disseminated distribution. In 9 cases, focal fibrosis with obliterations of alveoli prevailed. The extent of pathological results in the lungs does not correlate with the duration of artificial respiration. In cases of artificial respiration with pure oxygen, there is a special toxic component, which is illustrated by a young woman with polytraumatism who was administered artificial respiration for 5 weeks with pure oxygen. She died from respiratory insufficiency with severe pulmonary fibrosis. As different pathogenetic factors may cause irreversible pulmonary fibrosis, histomorphological classification is difficult later and, moreover, forensic problems result.     

人体颅脑贯通枪创后心肌和肺的超微结构观察

本文报告6例人体颅脑贯通枪创后2小时所取心肌和肺的超微结构变化。6例心肌及肺的超微结构基本相似。心肌最明显的变化是:Z 带排列不规则,灶性肌原迁维溶解,线粒体肿胀、基质电子密度降低和嵴消失,间质水肿。肺组织的明显变化是肺泡隔和肺间质增宽伴电子密度降低,肺泡隔毛细血管内中性粒细胞聚集,肺间质或肺泡腔内中性粒细胞浸润。本文对主要病理变化的意义和发生原理进行了讨论,认为肺间质水肿与神经源性肺水肿有关,由于伤后经过时间长短不同或有无颅内高压形成,而出现间质性水肿或肺泡内水肿。心肌的变化与缺氧有关。     

Lung histology in experimental drowning

Experiments were carried out on anesthetized rats which had to aspirate actively watery fluids of different osmolarities (range: freshwater--2.9% NaCl solution) by a tracheotomy tube. The cytologic and histological alterations which are to be found are mainly of osmotic origin. In aspiration of hypotonic solutions macroscopy shows the well-known emphysema aquosum. Corresponding to the structure of the respiratory system, the histological alterations show areolar limitations. The influx of fluids causes a wide range of reactions from the development of an alveolar-interstitial edema in combination with intracellular and intercellular vesiculation, karyolysis with swollen homogenized nuclei of the subendothelial, septal, and epithelial cells to a necrosis of all the cellular elements. A pronounced microangiopathy with edema of the vascular walls, a hydrops of the myocytes containing large vacuoles and perivascular edema with dilated lymphatic channels are likewise to be found. The alveolar macrophages are considerably increased. Sporadic ruptures of the alveolar walls and microhemorrhages occur. In salt water drowning alterations of the shape of both the erythrocytes (thorn-apple form) and the alveolar epithelium in combination with a striking of the pneumocytes and villous transformation prevail. Besides, these are capillary hyperemia and sludge. In a careful specimen analysis a differentiation of the findings between vital reactions and postmortem fluid impact is possible.     

A fatality caused by accidental production of hydrogen sulfide.

A 55-year-old male Caucasian truck driver was dead at the scene after breathing hydrogen sulfide (H(2)S) produced by an accidental transfer of sodium hydrogen sulfide (NaHS) from a tanker truck to a tank containing 4% sulfuric acid (H(2)SO(4)) and iron(II) sulfate (FeSO(4)). Autopsy of the decedent's body revealed pulmonary edema and passive congestion in lungs, spleen, kidneys, and adrenal glands. Postmortem biological samples were analyzed for carbon monoxide, cyanide, ethanol, and drugs. Since a potential exposure to H(2)S was involved, blood was also analyzed for sulfide (S(2-)). The analysis entailed isolating S(2-) from blood as H(2)S using 0.5M H(3)PO(4), trapping the gas in 0.1M NaOH, and determining the electromotive force using a sulfide ion specific electrode. Acetaminophen at a concentration of 14.3 microg/ml was found in blood, and metoprolol was detected in the blood, liver, and kidney samples. The blood S(2-) level was determined to be 1.68 microg/ml. It is concluded that the cause of death was H(2)S poisoning associated with a hazardous material accident in an industrial situation.     

Is the appearance of macrophages in pulmonary tissue related to time of asphyxia?

In order to connect the appearance of macrophages and giant cells in pulmonary tissue with the time of asphyxia the authors analyzed 50 asphyxiated human lungs paying their attention on the number of alveolar and interstitial macrophages and giant cells. They compared histological specimens of 25 asphixiated humans lungs following a slow asphyxia (30 min or more) with 25 histological specimens of asphyxiated human lungs following a rapid asphyxia (10-15 min). Alveolar and interstitial macrophages and giant cells per section, were considered and numbered. Controls were done on histological examination of traumatized lungs. In the pulmonary alveoli following on acute asphyxia there were 27.7+/-4.4 macrophages per section. Subjects dead after a slow asphyxiation showed 68.2+/-7.1 alveolar macrophages per section (p<0.001). Interstitial macrophages were also frequently present. No differences are detectable in the number of polynuclear giant cells between rapidly and slowly asphyxiated human lungs. The number of alveolar and interstitial macrophages per section can be considered as a further histological evidence of a slow asphyxia and can differentiate a slow asphyxia from an acute one.     

Exogenous Lipoid Pneumonia as a Contributory Factor in a Drug‐related Death

Postmortem investigation often reveals various conditions, which may or may not have played a part in the death of the individual. The case of a 32‐year‐old woman is reported, with a long history of drug addiction. She was found dead in her bed. The autopsy revealed diffuse pulmonary edema with congestion of the lungs, brain, liver, and spleen. Microscopic examination of the lungs showed multiple intra‐alveolar and interstitial foamy macrophages and extracellular fat droplets surrounded by polynuclear giant cells. Death was attributed to acute polydrug intoxication. As microscopic examination had revealed severe pulmonary lesions, lipoid pneumonia was considered as a contributing factor to death. Lipoid pneumonia is an uncommon entity with the characteristic radiograph features and histologic findings of alveoli filled with vacuolated, lipid‐laden histiocytes. It can be either exogenous or endogenous in cause, based on the source of the lipid. Exogenous lipoid pneumonia usually results from aspiration or inhalation of fat‐like material, such as mineral oil or petroleum‐based lubricants and decongestants, resulting in pulmonary inflammatory reactions.     

Determination of fetal age by immunohistochemical estimation of surfactant-producing alveolar type II cells.

We monitored the immunohistochemically determined amount of surfactant-producing alveolar type II cells in human fetal lung using polyclonal antibodies against apoprotein B and C of human pulmonary surfactant. Lungs of 30 dead-born fetuses without lung affection aged between 15 and 38 weeks of gestation were evaluated and the surface density of surfactant-producing alveolar type II cells was determined by morphometry. In lungs of fetuses with a gestational age less than 22 weeks no relevant number of positively reacting cells could be found. Between the 22nd and 29th week a progressive increase with considerable inter-individual variability was observed. From the 30th week on the number of the type II pneumocytes appeared rather constant without further significant increase. We provide evidence that the immunohistochemical detection of surfactant-producing alveolar type II cells is useful for the determination of the age of unknown and especially fragmented fetuses: The lack of surfactant-producing alveolar type II cells in fetal lungs before the 22nd week allows a rather safe distinction between fetal lungs of higher age from those of lesser age. Between the 22nd and 29th week an age-dependent increase in the number of these cells occurs with wide inter-individual variability allowing only an approximate age determination. In particular, this may be an important piece of information in fragmented fetal corpses. Furthermore, the number of surfactant-producing alveolar type II cells provides additional information on pulmonary maturation and may thus be helpful in the estimation of a theoretical survival chance.     

Death due to hydrofluoric acid

A case of death caused by an acid attack is presented. The victim, a young woman, was attacked by a person who threw acid onto her face. She reached the casualty department of a hospital where she died, a few hours later, from acute respiratory insufficiency due to the inhalation of acid vapors. The autopsy revealed severe chemical burns of her skin and lungs, with intense pulmonary hemorrhagic edema caused by the acid and its vapor. The subsequent chemical-toxicological analysis and the police investigation confirmed that death was due to hydrofluoric acid.     

Examinations to phenomenon of shock-lung (author's transl)]

The pathogenesis of shock lung as well as the success of therapy in this condition was studied in 79 cases of extrathoracic trauma. The water-, hemoglobin-, and DNA contents of the lungs were measured in order to determine the extent of edema, the rate of perfusion, and proliferation. The cases were divided into two groups according to whether they had or had not received medical therapy before death. The data from these two groups were compared using statistical methods in which time of survival was especially taken into account. The fluid balance, pO2, pCO2, central venous pressure, pH of the serum, total serum protein and serum creatinine were also studied in these cases. Results of the study are as follows. Three phases of the posttraumatic syndrome of shock-lung could be distinguished: phase I (initial phase): blood perfusion is increased, edema is beginning to form, and medical treatment has not yet begun. Phase II (early phase = sydrome of early respiratory failure): pulmonary edema is developing rapidly while perfusion is decreasing. Phase III (late phase = syndrome of late respiratory failure): proliferative changes predominante and the edema is still increasing. The mean weight of the lungs was 397 g (s = 170) in phase I, 774 G (S = 361) In phase II, and 1124 g (s = 310) in phase III. The survival times correlated significantly and positively with the amount of water and DNS in the lungs and significantly and negatively to the amount of hemoglobin in the lungs. Thus, increasing pulmonary edema and increasing proliferative changes occurred with decreasing pulmonary perfusion. This correlation was even noted in groups of patients who had not received medical treatment and whose survival times were short. In treated cases, the fluid balance was significantly and negatively correlated to the total serum protein.     

急性吗啡中毒大鼠主要器官内吗啡的免疫组化定位研究

一次静脉注射１２．５ｍｇ／ｋｇ。ｂｗ的盐酸吗啡染毒雄性Ｓ－Ｄ大鼠，２小时后处死，取其脑、肾、肝、肺、心组织以２％戊二醛和４％多聚甲醛混合液固定后，常规石蜡切片。运用抗吗啡抗血清及ＳＡＢＣ技术染色。结果显示上述组织切片有不同程度的阳性染色，阳性着色主要见于肾髓质部分肾小管上皮细胞，肝脏中央静脉周围的肝细胞、肺泡上皮细胞及肺内小支气管粘膜上皮细胞、中脑部分神经细胞、室管膜细胞、心肌细胞．以及各器官小血管及毛细血管内皮细胞胞浆、血浆及肾小管腔内尿液。     

多发性软组织挫伤后对肺及其他脏器的影响

目的观察多发性软组织挫伤后短时间内死亡案例的脏器病理学改变。方法应用常规组织学及免疫组织化学染色技术进行光学显微镜检查。结果光镜检查见肺组织毛细血管扩张充血，白细胞集聚，肺组织散在片状出血、灶状坏死及透明膜形成；心脏间质血管扩张充血，点灶状纤维溶解；脑组织充血水肿，肝脾充血。免疫组化发现肺泡腔及部分血管内纤维蛋白染色阳性，部分脾脏血管内及肾髓质集合管中肌红蛋白染色阳性。结论本研究结果提示多发性软组织挫伤后短时间内死亡的死因为成人呼吸窘迫综合征（ARDS）合并多脏器功能衰竭。     

Immunohistochemical study of blood group activities in severely burned human tissue

The blood, livers and lungs obtained from donors or cadavers of known blood groups were experimentally burned, while the temperatures inside the tissue specimens were automatically measured. All the distinguishable portions with various thermo-changes in each burned tissue specimen were examined for their blood-group activities A, B, Lea, Leb and P1 by means of the immunofluorescence and immunoperoxidase techniques. In the layer immediately before charring of the blood masses (tissue temperature: ca. 200-250 degrees C), the activities A, B, Lea, Leb and P1 could be specifically demonstrated on the erythrocyte membranes. In case of the burned livers and lungs, the A- and B-activities could be detected in the small blood vessels in the layer immediately before charring (ca. 200-250 degrees C), though the layer was so severely thermo-changed, that their original tissue structures could be no more observed. In the severely thermo-coagulated, porous and hardened layer of both organ tissues, the A- and B-activities could be demonstrated on the endothelial cells of the hepatic sinus and small blood vessels (especially in the alveolar walls). The simply thermo-coagulated inner portions well retained their original tissue structures and the A- and B-activities remained on the epithelial cells of the alveoli and bronchioles of the lung as well as the cells described above. The Lewis blood-group activities could be demonstrated on the epithelial cells of the bronchioles in the simply thermo-coagulated inner portion of the lung. The P1-activity could not be demonstrated in the burned tissues of the livers and lungs.     

Quantitative analysis of pulmonary pathophysiology using postmortem computed tomography with regard to the cause of death

Radiological lung transparency depends on the air contents involved in respiratory function. The present study quantitatively investigated postmortem lung air distribution in forensic autopsy cases (n=135) using computed tomography (CT) to analyze cardiopulmonary pathophysiology in the death process, involving emphysema, congestion and edema. Combined analyses of the CT morphology and attenuation value (Hounsfield unit, HU) of the bilateral lungs, with reference to histopathology, could categorize CT findings (10-90 percentile mode/mean HU values) with regard to the causes of death as follows: (I) hyperaeration (mode/mean HU below -760/-560: emphysema) for obstructive pulmonary disease, starvation and hypothermia (cold exposure); (II) mostly normal aeration with partial ground glass opacification (mode/mean HU, -850 to -360/-700 to -380: partial congestion and edema), consisting of subtype II-a with peri-bronchial/-vascular opacity for mechanical asphyxia, drowning and fire fatality, and subtype II-b with decreased vascularity for gunshot head injury, cerebrovascular disease and hemopericardium; (III) hypoaeration to airless with predominant hypostatic ground glass opacification (mode/mean HU, -870 to 0/-720 to -200: mottled hypostatic congestion and edema) for blunt head/neck injury, intoxication, hyperthermia (heat stroke) and congestive heart failure; (IV) hypoaeration to airless with predominant hypostatic consolidation (mode/mean HU, -790 to 0/-520 to -70: intense hypostatic congestion with edema) for acute ischemic heart disease; and (V) airless to consolidated (mode/mean HU over -420/-370: segmental or multiple patchy consolidations with edema) for pneumonia. Mode HU represents the major alveolar status, while the mean HU reflects the whole lung air contents. CT data analysis is useful for quantitative evaluation of pulmonary pathology as a supplementary procedure.     

Ventricular septal necrosis after blunt chest trauma

Ventricular Septal Defect (VSD) after blunt chest trauma is a very rare traumatic affection. We report here a case of blunt chest injury-related VSD and pseudoaneurysm. A 30-year old male truck driver was referred from a trauma center to our hospital seven days after a blunt chest trauma and rib fracture. The patient had severe pulmonary edema and echocardiography showed large VSD. Several mechanisms are involved in the pathogenesis of this affection including an acute compression of the heart muscle between the sternum and the spine, leading to excessive changes in the intrathoracic and most likely the intracardiac pressure after blunt chest injury. Traumatical patients with the same symptoms may be at risk of sudden death. Therefore, a high grade of suspicion is mandatory even without solid evidence of myocardial damage on the initial evaluation. In continue some hidden angles of this case was discussed. Given the prognostic implications of traumatic VSD with associated pseudoaneurysm, its detection has critical value for preventing its clinical sequelae.     

Ascertainment of the cause and tempo of death in forensic medical practice

In order to develop a method of ascertaining a cause of death and of evaluating its tempo the authors undertook a histological study and a study of a dehydration degree in 76 cases of death due to the below reasons: mechanical trauma, mechanical asphyxia, burn shock, and carbon monoxide intoxication. Acute emphysema of lungs, lack of edemas in lungs and brain, desquamation of pulmonary macrophages, hyperemia of renal capillaries, primary urine in some glomerules, prevalence of ischemic changes with karyopyknosis in medulla and hypohydration of brain were typical of fast death. Prevalence of dystelectasis in lungs, emptying of pulmonary capillaries, evident edema of lungs and brain, desquamation of pulmonary macrophages, lack of primary urine in glomerular capsules, acute circulatory disorders of renal hemodynamics with sweating of fibrin and erythrocyte glomerules into cavities, necrotic nephrosis, pigment cylinders in renal tubules, thrombi in vessels, prevalence of chromatolysis, karyolysis and cytolysis in medulla, pronounced glial reaction as well as pronounced edema of brain and its hyperhydration were typical of slow death.     

Sudden infant death from atelectasis due to amniotic fluid aspiration

An infant girl, whose hands showed lobster-claw deformity, was found dead in her bed at 17 days of age. Macroscopic and microscopic examination of the lungs showed fatal atelectasis. The alveolar spaces were filled with fluid, epithelial cells, and squamous debris. These were the constituents of amniotic fluid aspirated before birth. The present case suggested that some sudden unexpected deaths in early infancy are delayed deaths caused by amniotic fluid aspiration.     

Quantitative analysis of pulmonary neuroendocrine cell distribution of the fetal small airways using double-labeled immunohistochemistry

Pulmonary neuroendocrine cells (PNECs) are supposed to play an essential role in development of fetal lung and neonatal respiratory adaptation. Some previous studies have suggested the close relation between PNECs and sudden infant death syndrome (SIDS). To investigate how PNECs distribute to the thermal bronchioli of fetal lung may be a clue to clarify this relation. Since it is difficult to distinguish bronchiole from alveolus in fetal lung, we performed double immunostaining with antibody against chromogranin A (CGA) and alpha-smooth muscle actin (SMA) which can make clear distinction between them. In this study, formalin-fixed, paraffin-embedded lung tissues from 18 autopsy cases from 16 to 28 weeks of gestation were assessed. CGA immunopositive cells were counted and the length of basement membranes of terminal bronchioli was measured with computed image analyzer. Density of PNECs was expressed as the number of immunopositive cells per millimeter of basement membrane. Terminal bronchiole stained with SMA was clearly distinguished from alveolus at 16 weeks. With gestational age, CGA immunopositive PNECs were gradually increased in 2 folds by the 25th week. After that, their density wasn't changed significantly until termination. It is suggested that PNECs in terminal bronchiole was playing an important role in morphogenesis of alveolar ducts and alveolar sacks.     

An unusual case of high-voltage electrocution of a truck driver due to inadvertent contact of the truck with an overhead wire

Electrocution deaths are mostly accidental. However, reconstruction of events in unusual electrocution death is challenging. This article reports an accidental death due to electrocution in a highly unusual circumstance, in which a truck driver reversing his vehicle was electrocuted when his truck inadvertently touched an overhead high-voltage wire. The electric injury marks were present over the sole of the right foot. The scene investigation revealed that the high-voltage wire was loose and was below the level of the prescribed height. The truck was passing over an elevated area made up of dirt and stone. The interior of the cabin of the truck revealed a few non-insulated metallic areas over the floor of the truck, between the accelerator and the brake, which were attributed as the sources of entry of electricity into the body. The electric injury marks were different than those usually seen in high-voltage electrocution as there was an intermediate object (truck) involved, and the contact period between the truck and the electric wire was minimal. This fatality was attributed to the non-proper insulation of the interior of the truck, the negligent driving of the truck driver over the elevated surface, and the loose high-voltage wire without proper maintenance.