Two Fatal Cases of Hidden Pneumonia in Young People*

Abstract: Acute respiratory distress syndrome (ARDS) is a severe lung disease characterized by inflammation of the lung parenchyma leading to impaired gas exchange. This condition is often lethal, usually requiring mechanical ventilation and admission to an intensive care unit. We present two fatal cases of hidden pneumonia in young people and discuss the pathophysiological mechanism of ARDS with reference to the histological pattern. A complete forensic approach by means of autopsy and histological, immunohistochemical, and microbiological, examination was carried out. In both cases the cause of death was cardio‐respiratory failure following an acute bilateral pneumonia with diffuse alveolar damage and ARDS associated with sepsis and disseminated intravascular coagulation. Our cases suggest on one side the importance of an early diagnosis to avoid unexpected death while on the other that the diagnosis of ARDS has to be confirmed on the basis of a careful postmortem examination and a complete microscopy and microbiological study.     

多发性软组织挫伤后成人呼吸窘迫综合征──组织学及免疫组织化学研究

本研究应用组织学Ｈ·Ｅ、Ｍａｌｌｏｒｙ、ＰＴＡＨ以及免疫组织化学染色方法对６例多发性软组织挫伤后成人呼吸窘迫综合征者肺组织改变进行了深入探讨。结果表明，所有外伤性呼吸窘迫综合征者肺组织均呈急性充血、出血及水肿改变，且免疫组织化学染色证明，水肿液中含有纤维蛋白（原）成份。在６例中２例可见肺组织局灶性出血坏死，３例有散在性血管内纤维蛋白柱形成及肺泡内透明膜形成。这些改变均属成人呼呼吸窘迫综合征的早期肺损伤。对多发软组织挫伤后呼吸窘迫综合征的形成机理进行阐述。     

Cerebral traumatism with a playground rocking toy mimicking shaken baby syndrome

Shaken baby syndrome (SBS), one of the most deadly and devastating forms of child abuse, is caused by violent shaking. The combination of subdural hematoma, retinal hemorrhage, brain swelling, and diffuse axonal injury is highly typical of this syndrome and faced with these autopsy findings, induced traumatic lesions are strongly considered. However, it is known that motor-vehicle accidents and falls from great height can also produce this pattern of injury. Nevertheless, stories of arms fall, couch fall, or bumped head while the baby is being carried are generally considered incompatible with SBS. We here report a case of a 2-year-old boy presenting with all the classic autopsy findings of SBS from a playground rocking toy shaken by an older child.     

Barotrauma and air embolism in hyperbaric oxygen therapy

A 69-year-old woman underwent hyperbaric oxygen therapy because of a nonhealing ulcer of her foot. During decompression, she developed a left-sided hemiplegia and confusion. Recompression resulted in transient neurologic improvement, but she eventually became comatose. Ventricular dysrhythmias developed and she died without regaining consciousness 17 h after onset of symptoms. An autopsy revealed diffuse interstitial pulmonary fibrosis with severe paracicatricial emphysema, chronic interstitial inflammation, and chronic bronchitis with abundant intrabronchial mucus. There was extensive multifocal ischemic injury of the cerebral cortex. The hippocampi, basal ganglia, and cerebellum were spared. Scattered acute myofiber necrosis was present in the heart. Clinical presentation and autopsy findings strongly support the diagnosis of air embolism and illustrate a potential risk of hyperbaric oxygen therapy in patients with preexisting pulmonary disease.     

Sudden Death Due to Undiagnosed Rheumatic Heart Disease in a Child

We report the case of a 5‐year‐old boy who died from complications of rheumatic heart disease with atypical presentation. He was hospitalized for recent inflammatory and neurological symptoms. He was diagnosed with viral encephalitis. He died the day after he was discharged. The macroscopic autopsy findings were unremarkable. Histology revealed typical rheumatic heart disease. Neuropathology showed cerebral infarction due to an embolic event linked with the rheumatic valvulitis. The cause of death was determined as heart failure due to rheumatic heart disease secondary to an undiagnosed acute rheumatic fever. It is related to an autoimmune response to infection with group A streptococcus. It mainly affects children in developing countries. In our case, viral encephalitis was consistent with the medical history and the proper diagnosis was made on histological analysis. Forensic pathologists should consider this diagnosis facing a sudden unexpected death in childhood, even in industrialized countries.     

我国首例艾滋病抗体阳性死亡病例的进一步病理研究

作者原报告艾滋相关综合征(ARC),经用组化和免疫组化方法,发现肺部有混合性机会感染和淋巴结免疫缺陷病变,应诊断艾滋病(AHDS)。     

Death Caused by Toxic Epidermal Necrolysis (Lyell Syndrome)

Abstract: Toxic epidermal necrolysis (TEN) is characterized by fever, scalded appearance of the skin, and epidermolysis associated to blister formation and exfoliation, and it is caused by hypersensitivity reaction to a drug. The authors report two cases of death as a result of TEN; both referred to old aged women treated with a polytherapy including allopurinol. Both patients displayed erythematous skin lesions similar to scald burns and epidermolysis at the face, chest, and abdomen and died shortly after hospitalization. Autopsy findings and histological examinations revealed epidermal necrolysis and confirmed the clinical diagnosis. A strict time‐correlation between allopurinol administration and symptoms was evidenced. Because of its iatrogenic origin, TEN often arises suspicions of medical liability; however, because of its unpredictable nature, the occurrence of this syndrome cannot be ascribed to the medical staff whose main task is the rapid diagnosis and the correct management.     

Fat embolism syndrome associated with atraumatic compartment syndrome of the bilateral upper extremities: An unreported etiology

Fat embolism syndrome (FES) is a potentially life-threatening condition that develops when fat embolism leads to clinical symptoms and multisystem dysfunction. The classic triad of respiratory distress, neurologic symptoms, and petechial rash are non-specific, and the lack of specific laboratory tests makes the diagnosis of FES difficult. Although FES is most common after long bone fractures, multiple conditions some of which are atraumatic have been associated with the development of FES. We report a case of FES that occurred in the setting of a non-traumatic compartment syndrome of the upper extremities. The pathologic and clinical findings, pathophysiology, diagnostic challenges, and pathologic methods to properly diagnose FES are discussed with a review of the relevant literature. This case highlights the importance of the autopsy in making a diagnosis of FES in cases where death could otherwise be incorrectly attributed to multi-organ system failure, shock, or sepsis.     

Medical responsibility in the operating room: the example of an amniotic fluid embolism

Amniotic fluid embolism (AFE) continues to be one of the most feared complications of pregnancy. A healthy 32-year-old woman died during delivery after a normal 39-week third pregnancy. The family filed a complaint with a criminal court as the causes of death appeared unclear. No risk factor associated with AFE was identified. Clinical presentation was typical, including sudden onset of cardiovascular and respiratory symptoms. Autopsy confirmed the histological diagnosis of amniotic embolism and excluded an iatrogenic cause of death or anesthetic malpractice. This article highlights the value of both antemortem records and histological features in establishing the diagnosis of AFE and demonstrates the fundamental importance of autopsy in an unexpected death related directly or indirectly to a medical procedure.     

Influenza A virus infection complicated by fatal myocarditis

Influenza virus typically causes a febrile respiratory illness, but it can present with a variety of other clinical manifestations. We report a fatal case of myocarditis associated with influenza A infection. A previously healthy 11-year-old girl had malaise and fever for approximately 1 week before a sudden, witnessed fatal collapse at home. Autopsy revealed a pericardial effusion, a mixed lymphocytic and neutrophilic myocarditis, a mild lymphocytic interstitial pneumonia, focal bronchial/bronchiolar mucosal necrosis, and histologic changes consistent with asthma. Infection with influenza A (H3N2) was confirmed by virus isolation from a postmortem nasopharyngeal swab. Attempts to isolate virus from heart and lung tissue were unsuccessful. Immunohistochemical tests directed against influenza A antigens and in situ hybridization for influenza A genetic material demonstrated positive staining in bronchial epithelial cells, whereas heart sections were negative. Sudden death is a rare complication of influenza and may be caused by myocarditis. Forensic pathologists should be aware that postmortem nasopharyngeal swabs for viral culture and immunohistochemical or in situ hybridization procedures on lung tissue might be necessary to achieve a diagnosis. Because neither culturable virus nor influenza viral antigen could be identified in heart tissue, the pathogenesis of influenza myocarditis in this case is unlikely to be the result of direct infection of myocardium by the virus. The risk factors for developing myocarditis during an influenza infection are unknown.     

Pathological spectrum of the lung in cases of violent death: Part II. Clinicopathologic correlation

The correlation between the type of pathological lesion of the lung and the circumstances which encompass their evolution in 66 cases of violent death have been examined. Pulmonary lesions have been classified into four groups. 1. Inflammatory alveolar lesions without a diffuse interstitial involvement (IAL) which result from direct aggressions in subjects of advanced age. 2. Inflammatory alveolar lesions with a diffuse interstitial affectation (IALW) which are more frequent in younger subjects having a higher defense capacity and with severe lesions requiring admission to an intensive care unit. 3. Edemohemorrhagic lesions (EHL) appearing as a precocious lesion at any age. 4. Unspecific chronic lesions (UCL) previous to the aggression and without any relationship to death. The most obvious feature noted was the frequent occurrence of certain types of acute pulmonary lesions indicative of the rapid and extensive capacity of the lung to react to a lesion agent even when death follows rapidly after the aggression. The scarcity of acute interstitial lesions among the older group can be related to a diminution of biological defense activity leading to a less vigorous response; on the contrary, diffuse lesions of the wall seem to be related to an excess of defense mechanisms, determined more by age, severity of lesion, and type of medical assistance received than by a specific type of aggression.     

Asplenia as a cause of sudden unexpected death in childhood

Sudden unexpected death in childhood is rare. The commonest causes of such deaths are a result of fulminating infections of the respiratory or nervous systems. Other causes include unsuspected congenital abnormalities of the heart, acute metabolic disorders, and rarities such as internal hemorrhages and pulmonary thrombosis. Recognition of children with congenital asplenia who are otherwise normal but have an increased susceptibility to overwhelming sepsis is extremely difficult. We reviewed 1763 autopsy files from our institution over 5 years (1990-1995), of which 293 were classified as pediatric cases. The vast majority of the cases were stillbirths and deaths within the first year of life as a result of complex congenital anomalies. Four cases of asplenia were identified in our entire series, 3 of which were of the congenital syndromal variety and 1 of which was a case of isolated sporadic congenital asplenia. All 4 cases of asplenia were analyzed in detail with respect to autopsy findings and cause of death. Severe complex cardiac malformations were present in the congenital syndromal asplenia patients; these other malformations contributed significantly to their death. In this report, we discuss in detail the autopsy findings in a previously healthy 4-year-old girl who presented with a brief 8-hour history of being unwell and died within 4 hours of admission into the hospital. She had sporadic, isolated congenital asplenia complicated by high-grade type 6B pneumococcemia and acute bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome). Previously healthy children who clinically deteriorate very rapidly should have a blood smear done as part of their clinical workup. The detection of Howell-Jolly bodies on a peripheral blood smear can be an indicator of asplenia, and this diagnosis can be confirmed by medical imaging of the abdomen. Such steps may aid in the aggressive management of isolated congenital asplenia and thereby avert untimely death.     

Forensic medicine and morphologic aspects of fatal amniotic fluid aspiration

The massive aspiration of amniotic fluid as one cause of a fatal postpartal asphyxia will be demonstrated under the aspect of preliminary criminal law proceedings against physicians because of medical negligence. The pathomorphologically established diagnosis of a fatal aspiration of amniotic fluid supposes extensive and systematic quantitative histological examination of both lungs. The technique of histological cross sections through the entire lung combined with morphometry is a suitable method to exactly record the alterations of bronchi and lung parenchyma by aspiration of amniotic fluid and their complications, such as interstitial emphysema.     

A comparison of respiratory symptoms and inflammation in sudden infant death syndrome and in accidental or inflicted infant death

Upper respiratory infection and pulmonary inflammation are common in sudden infant death syndrome, but their role in the cause of death remains controversial. Controlled studies comparing clinical upper respiratory infection and inflammation in sudden infant death syndrome with sudden infant deaths caused by accidents and inflicted injuries (controls) are unavailable. Our aim was to compare respiratory inflammation and upper respiratory infection within 48 hours of death and postmortem culture results in these two groups. A retrospective analysis of upper respiratory infection and pathologic variables in the trachea and lung of 155 infants dying of sudden infant death syndrome and 33 control infants was undertaken. Upper respiratory infection was present in 39% of sudden infant death syndrome cases and 40% of control cases. Upper respiratory infection was more likely to have occurred in association with more severe lymphocytic interstitial pneumonitis when sudden infant death syndrome cases and control cases were combined ( P=.04). Proximal and distal tracheal lymphocytic infiltration was more severe in control cases than in sudden infant death syndrome cases ( P=.01 and.01, respectively). Lymphocytic infiltrations of the bronchi, bronchioles, and pulmonary interstitium were similar between groups. Bronchial associated lymphoid tissue was more prominent in control cases ( P=.04). Cultures were positive in 80% of sudden infant death syndrome cases, 78% of which were polymicrobial. Among control cases, 89% were positive, with 94% being polymicrobial. This study confirms that microscopic inflammatory infiltrates in sudden infant death syndrome are not lethal.     

Fatal neurotoxic response to neuroleptic medications: case report and review of the literature

Neuroleptic malignant syndrome (NMS) is a diagnosis of exclusion difficult to make due to a lack of pathognomonic features. Diagnosing NMS by postmortem examination becomes increasingly challenging when possible underlying brain pathology is obscured. The diagnosis is based on clinical history and laboratory findings. Autopsy and histologic findings, if any, usually are reflective of hyperthermia or complications (eg, aspiration pneumonia) of NMS. The authors describe a case of a 36-year-old Hispanic woman with a presumptive diagnosis of pseudoseizures, treated with various combinations of neuroleptic medications over a 6-week period prior to her sudden, unexpected, in-hospital death. Neuroleptic malignant syndrome is likely to have contributed to this patient's death. Confounding factors and medicolegal issues of a postmortem diagnosis of NMS are discussed.     

Cardiomyopathies—Misdiagnosed as Sudden Infant Death Syndrome (SIDS)

Cardiomyopathies are an important and heterogenous group of diseases. With the identification of several new disease entities over the past decade, advances in diagnosis and precise causation, some disease definitions have become outdated. The past decade has witnessed a rapid evolution of molecular genetics in cardiology, e.g. myocardial diseases (Hypertrophic cardiomyopathy—HCM, Arrhythmogenic right ventricular cardiomyopathy—ARVCM) and channelopathies (Long QT syndrome—LQTS, Brugada syndrome—BrS, Catecholaminergic Polymorphic Ventricular Tachycardia—CPVT and Short QT syndrome—SQTS) as diseases predisposing to potentially lethal ventricular tachyarrhythmias. Beside the detection of mutations in several genes, histological and immunohistochemical findings can point to a cardiomyopathy as underlying disease. Therefore, previous microscopical investigations of different parts of the myocardium can help to select those cases of suspected Sudden Infant Death Syndrome (SIDS), where a search for genetic mutations can lead to a diagnosis explaining the sudden and unexpected death.     

Fatal outcome in a case of pontocerebellar hypoplasia type 2

Pontocerebellar hypoplasia (PCH) is a very rare congenital (autosomal recessive) condition with fetal onset. Only a few cases have been published on the basis of both clinical data (symptoms/neuroradiological imaging) and autopsy results. This paper reports on such a case involving a 1.5-year-old male infant. The child suffered from severe psychomotor delay, extrapyramidal dyskinesia and epileptic seizures, but did not exhibit signs of spinal muscular atrophy as related to PCH type 1. Magnetic resonance imaging (MRI) at the age of 6 months demonstrated olivo-pontine and bilateral cerebellar hypoplasia. The boy was unexpectedly found dead. Autopsy disclosed a severe aspiration of gastric contents as the final cause of death. The neuropathological examination confirmed PCH type 2 (according to Barth [Brain Dev., 15 (1993) 411-422]) with marked microcephaly and olivopontocerebellar hypoplasia. Histologically, decreased density of olivo-pontine neurons, reduction of granular and Purkinje's cell layers of the cerebellum, slight astroglial proliferation and fragmented appearance of the dentate nuclei were observed. The immunohistochemical expression pattern was determined using antibodies against glial fibrillary acidic protein, synaptophysin and neurofilament protein. Summarizing, typical features of PCH type 2 were present and proved by clinical course, MRI and autopsy. Despite severe symptoms due to a natural disease this rare neurogenetic entity can become of forensic interest, when sudden unexpected death occurs.     

冠状病毒感染性疾病尸体检验相关病原学检测回顾与展望

冠状病毒曾经给世界带来两次严重的人类间大流行,包括严重急性呼吸综合征(severe acute re?spiratory syndrome,SARS)和中东呼吸综合征(Middle East respiratory syndrome,MERS),2019年岁末新型冠状病毒肺炎(coronavirus disease 2...     

Identification of mechanical asphyxiation in cases of attempted masking of the homicide

Five homicides are described that had remained unexplained as to the causes of death after gross pathology. Although general signs of asphyxiation were present, they were lacking injuries specific of strangulation or oro-nasal occlusion. The diagnoses of asphyxiation were established by microscopical investigation of the lung and confirmed by subsequent police inquiries. An oro-nasal occlusion was involved in three cases, a strangulation or an oro-nasal occlusion, in another case. The victims were young and healthy. Toxicological investigations remained negative in four cases; one victim was anaesthetized by bromazepam and ether and had a blood alcohol concentration of 80 mg/100 ml. Lung histology and electron microscopy revealed acute emphysema, the development of a haemorrhagic-dysoric syndrome and a microembolism syndrome. With regard to the haemorrhagic-dysoric syndrome, the development of alveolar-interstitial edema is particularly important. This finding may also be diagnosed by light microscopy in semi-thin sections. It is emphasized that the combined action of several pathomechanisms is responsible for the rapid manifestation of the pulmonary lesions. Especially, the haemorrhagic-dysoric syndrome is brought about by the combined action of inspiratory intrapulmonary vacuum and raised intracapillary pressure. The complex pattern allows to compile the diagnosis of mechanical asphyxia even if there is no corresponding injury.     

Maternal death due to non-traumatic fat embolism

The aim of this report is to document a case of non-traumatic fat embolism (NTFE) and to address the need for considerition of fat embolism in suspicious deaths resulting from respiratory distress in the postpartum period. A 28-years-old woman autopsied at the Morgue Department of the Council of Forensic Medicine is included to the study. This female became unconscious and developed respiratory distress 4 h after delivery, and this was followed by respiratory arrest. External examination revealed resuscitation marks and normal postmortem changes. Light microscopy revealed massive fat embolization involving most of the alveolar capillaries on several sections. Only in one particular area was a bone marrow embolus. Pathological diagnosis of the lung was diffuse pulmonary fat embolism. There was no evidence of other organ involvement with emboli. Other visceral organs showed no striking findings other than mild congestion. The cause of death was considered to be respiratory insufficiency resulting from severe fat embolism of the lungs.