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Necrotizing fasciitis (NF) is a life-threatening infection of soft tissues spreading along the fasciae to the surrounding musculature, subcutaneous fat and overlying skin areas that can rapidly lead to septic shock and death. Due to the pandemic increase of medical malpractice lawsuits, above all in Western countries, the forensic pathologist is frequently asked to investigate post-mortem cases of NF in order to determine the cause of death and to identify any related negligence and/or medical error. Herein, we review the medical literature dealing with cases of NF in a post-mortem setting, present a case series of seven NF fatalities and discuss the main ante-mortem and post-mortem diagnostic challenges of both clinical and forensic interests. In particular, we address the following issues: (1) origin of soft tissue infections, (2) micro-organisms involved, (3) time of progression of the infection to NF, (4) clinical and histological staging of NF and (5) pros and cons of clinical and laboratory scores, specific forensic issues related to the reconstruction of the ideal medical conduct and the evaluation of the causal value/link of any eventual medical error.

After attending this presentation, attendees will be aware of a new application of micro-Computed Tomography (CT) for dealing with the identification of the signs of pressure of the neck in cases of subtle manual strangulation. This presentation will impact the forensic science community by suggesting a novel approach for the identification of laryngeal fractures by means of micro-CT analysis. It is widely accepted that there are no specific or fully determinate signs of asphyxia. In cases of subtle fatal neck compression, postmortem findings on external examination of a body as well as on autopsy may vary considerably depending on the type of violent trauma, the strength of the resistance exerted by the victim, and on the intensity and duration of neck compression. Based on the detection of a combination of morphological hallmarks such as external injuries to the skin, hyoid or laryngeal fractures, hemorrhages of the overlying soft tissues, and subconjuctiveal petechiae, the diagnosis of homicidal neck compression is generally accepted. A case is presented of a 45-year-old schizophrenic patient found on the floor of the bedroom of a psychiatric ward in cardiopulmonary arrest. The patient was successfully resuscitated; nevertheless, brain death was declared after two days in a vegetative state. The roommate of the deceased, who was also schizophrenic, stated that “the voice of God told me to kill my roommate” and death occurred after a prolonged scuffle. The body showed only vague signs of violence at external inspection (i.e., a subtle bruise on the forehead and a minute scratch on the left arm). At autopsy, the identification of subepicardial petechiae and moderate pulmonary emphysema were not useful for the diagnosis of asphyxial death because these signs might be related to resuscitative maneuvers with prolonged artificial ventilation. Since focal hemorrhagic infiltration of the tracheal mucosa and the superior horns of the thyroid cartilage were observed, a CT scan of the entire larynx was performed, with the goal of identifying laryngeal fractures. Moreover, both superior horns of the thyroid cartilage were analyzed thorough a micro-CT, a radiological technique for tissue analysis with a spatial resolution of a few microns. The 3D reconstruction allowed for identification of multiple cartilage fragments of the larynx. Consequently, the cause of death was identified as asphyxia due to manual strangulation. Considering that micro-CT analysis is able to generate images with a high level of detail compared to conventional radiological techniques, in cases of subtle fatal neck compression this type of investigation could be useful for the morphological identification of comminuted bilateral fractures. This may be particularly useful in cases involving children and young adults where fractures or cartilage damages may be minimal or absent as a consequence of the elasticity of the ligaments around the larynx and hyoid bone as well as the early stage of ossification.

Hydranencephaly is a severe congenital condition where most of the cerebral hemispheres are replaced by a membranous sac. Despite the growing amount of case reports, most pathogenic, phenotypic, and prognostic aspects of hydranencephaly remain controversial. By matching the recent literature data with the findings of our own series (four cases: two fetuses at the twelfth gestational week, a 32-year-old man, and a 14-year-old female), we attempted to date back the insult leading to hydranencephaly to understand its pathogenesis and to explain the basis of its protean phenotype. The variable detection of cerebral remnants seems to mirror the developmental pathway of cerebral arteries. Moreover, fetal and postnatal neuroimaging data and histopathologic findings point toward an early bilateral internal carotid artery occlusion, mostly occurring between the eighth and twelfth gestational weeks, as the main pathogenic mechanism of hydranencephaly.

Objective To report an ataxic variant of Alzheimer disease expressing a novel molecular phenotype. Design Description of a novel phenotype associated with a presenilin 1 mutation. Setting The subject was an outpatient who was diagnosed at the local referral center. Patient A 28-year-old man presented with psychiatric symptoms and cerebellar signs, followed by cognitive dysfunction. Severe β-amyloid (Aβ) deposition was accompanied by neurofibrillary tangles and cell loss in the cerebral cortex and by Purkinje cell dendrite loss in the cerebellum. A presenilin 1 gene (PSEN1 ) S170F mutation was detected. Main Outcome Measures We analyzed the processing of Aβ precursor protein in vitro as well as the Aβ species in brain tissue. Results The PSEN1 S170F mutation induced a 3-fold increase of both secreted Aβ 42 and Aβ 40 species and a 60% increase of secreted Aβ precursor protein in transfected cells. Soluble and insoluble fractions isolated from brain tissue showed a prevalence of N–terminally truncated Aβ species ending at both residues 40 and 42. Conclusion These findings define a new Alzheimer disease molecular phenotype and support the concept that the phenotypic variability associated with PSEN1 mutations may be dictated by the Aβ aggregates' composition.

Aluminum lactate [Al(lact)3] (hydrophilic, hydrolytically unstable) and aluminum acetylacetonate [Al(acae)3] (lipophilic, hydrolytically stable) were tested as potential toxicants to rabbits upon IV administration both as aqueous solutions and as liposome suspensions. Both chemicals behaved as cardiotoxic agents when administered as aqueous solutions, but Al(acae)3 was at least two orders of magnitude more active than Al(lact)3. Al(acae)3, but not Al(lact)3, caused myocardial infarcts resembling those in humans (with contraction bands) at doses as low as 0.24 mg/kg body weight, as well as a prominent acanthocytosis. Al(lact)3, when administered as a liposome suspension, was about 300 times more toxic than in aqueous solution, although cardiac damage was not infarctual in character. Both chemical and physical speciation of aluminum(III) thus play an essential role in determining the toxicity of the metal. Images FIGURE 2. FIGURE 3.

Sixteen patients (one with tuberculoma of the anterior optic pathways, the other 15 with opto-chiasmatic arachnoiditis) are presented. They are divided into three categories (definite, likely, possible) from the point of view of the pathogenetic link of their optic pathology with a primary tuberculous infection. Neurosurgical treatment had a positive effect upon the visual symptoms in five patients (31.25%), no effect in three cases (18.75%); in the other eight patients (50%) it could not prevent progression of visual impairment.

The clinicopathologic picture of a case of so-called 'sarcoglioma' is reported. This tumor is characterized by a core of sarcomatous tissue, surrounded by an area of gradual transition from reactive to neoplastic glial cells; it occurs in children or in young adults and is very rare in comparison with the secondary sarcoma deriving from the vascular component of a glioblastoma (so-called 'gliosarcoma'). The clinical and laboratory features and the pathology of this case are discussed in detail.