Ετικέτες

Σάββατο 29 Δεκεμβρίου 2018

The Short Treatment Allocation Tool for Eating Disorders: current practices in assigning patients to level of care

Abstract

Objective

The Short Treatment Allocation Tool for Eating Disorders (STATED) is a new evidence-based algorithm developed to match patients to the most clinically appropriate and cost-effective level of care (Geller et al., 2016). The objective of this research was to examine the extent to which current practices are in alignment with STATED recommendations.

Method

Participants were 179 healthcare professionals providing care for youth and/or adults with eating disorders. They completed an online survey and rated the extent to which three patient dimensions (medical stability, symptom severity, and readiness) were used in assigning patients to each of five levels of care.

Results

The majority of analyses testing a priori hypotheses based on the STATED were statistically significant (all p's < .001), in the direction of STATED recommendations. However, a strict coding scheme evaluating the extent to which ratings were fully consistent with the STATED showed inconsistency rates ranging from 17 to 55% across the five levels of care, with the greatest inconsistencies involving the use of readiness information, and the lowest involving the use of medical stability information.

Discussion

Although practices were generally aligned with the STATED recommendations, readiness information was used least consistently in assigning patients to level of care.



http://bit.ly/2BM8hAI

Issue Information



http://bit.ly/2EXXqXD

Editorial



http://bit.ly/2EWnQK4

Botulinum toxin blocks mast cells and prevents rosacea like inflammation

Publication date: Available online 28 December 2018

Source: Journal of Dermatological Science

Author(s): Jae Eun Choi, Tyler Werbel, Zhenping Wang, Chia Chi Wu, Tony L. Yaksh, Anna Di Nardo

Abstract
Background

Rosacea is a chronic inflammatory skin condition whose etiology has been linked to mast cells and the antimicrobial peptide cathelicidin LL-37. Individuals with refractory disease have demonstrated clinical benefit with periodic injections of onabotulinum toxin, but the mechanism of action is unknown.

Objectives

To investigate the molecular mechanism by which botulinum toxin improves rosacea lesions.

Methods

Primary human and murine mast cells were pretreated with onabotulinum toxin A or B or control. Mast cell degranulation was evaluated by β-hexosaminidase activity. Expression of botulinum toxin receptor Sv2 was measured by qPCR. The presence of SNAP-25 and VAMP2 was established by immunofluorescence. In vivo rosacea model was established by intradermally injecting LL-37 with or without onabotulinum toxin A pretreatment. Mast cell degranulation was assessed in vivo by histologic counts. Rosacea biomarkers were analyzed by qPCR of mouse skin sections.

Results

Onabotulinum toxin A and B inhibited compound 48/80-induced degranulation of both human and murine mast cells. Expression of Sv2 was established in mouse mast cells. Onabotulinum toxin A and B increased cleaved SNAP-25 and decreased VAMP2 staining in mast cells respectively. In mice, injection of onabotulinum toxin A significantly reduced LL-37-induced skin erythema, mast cell degranulation, and mRNA expression of rosacea biomarkers.

Conclusions

These findings suggest that onabotulinum toxin reduces rosacea-associated skin inflammation by directly inhibiting mast cell degranulation. Periodic applications of onabotulinum toxin may be an effective therapy for refractory rosacea and deserves further study.



http://bit.ly/2Rk4jcm

Incorporating reference guided priors into calibrationless parallel imaging reconstruction

Publication date: Available online 28 December 2018

Source: Magnetic Resonance Imaging

Author(s): Qingyong Zhu, Wei Wang, Jing Cheng, Xi Peng

Abstract
Purpose

To propose and evaluate a new calibrationless parallel imaging method aimed at further improving the reconstruction accuracy of the accelerated multi-channel MR images.

Method

We introduce a new calibrationless parallel imaging method. On top of exploiting joint sparsity cross channels of the target image to be reconstructed, it incorporates similar priors on the grey-level intensity and edge orientation, which both come from a high-spatial resolution reference image that can be easily obtained in many clinical MRI scenarios. The mixed l2-l1 norm is used to enforce joint sparsity and a multi-scale gradient orientation operator is applied to extract fine edges from the reference image. Additionally, this optimization problem can be solved via a non-linear conjugate gradient algorithm with line search in this work.

Results

The proposed method is compared with the existing state-of-the-art auto-calibration and calibrationless parallel imaging techniques. The experiments on different in-vivo brain MR datasets show that the proposed method has the superior performance in terms of both artifacts suppression and details preservation.

Conclusion

The reference guided calibrationless parallel imaging method can significantly improve the performance of joint reconstruction of target channel images. Even when the reduction factor is high, it can keep edge structures well.



http://bit.ly/2AiLSuM

Right hemisphere superiority for executive control of attention

Publication date: Available online 29 December 2018

Source: Cortex

Author(s): Alfredo Spagna, Tae Hyeong Kim, Tingting Wu, Jin Fan



http://bit.ly/2rVw10G

18F-choline PET/CT incidental thyroid uptake in patients studied for prostate cancer

Abstract

Purpose

Thyroid incidental uptake is defined as a thyroid uptake incidentally detected by imaging examinations performed for non-thyroid disease. The aim of this study was to establish the prevalence and the pathological nature of focal thyroid incidental uptake (FTIU) among patients studied with 18F-choline-PET/CT.

Materials and methods

We retrospectively evaluated 368 patients who performed 18F-choline-PET/CT between June 2016 and August 2018. The PET images were analyzed visually and semi-quantitatively by measuring the maximum standardized uptake value (SUVmax) and the mean SUV (SUVmean) of the thyroid gland and of the FTIU; every focal thyroid uptake deviating from physiological distribution and background was considered FTIU. Final diagnosis of FTIU was obtained by cytological or histological examination after surgery.

Results

The average SUVmax and SUVmean of thyroid gland in population were 3 and 1.8. Among 368 patients, FTIU was identified in nine cases (2.4%) and eight underwent further investigations to determine the nature. Two FTIU were classified as malignant (thyroid carcinoma), whereas five were benign (three nodular hyperplasia, one follicular adenoma, one Hurtle cell adenoma) and one indeterminate at cytological examination. In malignant lesions, average SUVmax was 9.6 and 4.5, respectively, while average SUVmean was 5.3 and 2.9, respectively. Average SUVmax and SUVmean of benign lesions were 4.9 and 3.2 and of the indeterminate lesion 5 and 3, respectively.

Conclusions

18F-choline-PET/CT FTIU may be a relevant diagnostic reality, which requires further investigations and affects management, especially considering that, despite being mainly benign, also malignancy is possible.



http://bit.ly/2ETjhPI

18F-choline PET/CT incidental thyroid uptake in patients studied for prostate cancer

Abstract

Purpose

Thyroid incidental uptake is defined as a thyroid uptake incidentally detected by imaging examinations performed for non-thyroid disease. The aim of this study was to establish the prevalence and the pathological nature of focal thyroid incidental uptake (FTIU) among patients studied with 18F-choline-PET/CT.

Materials and methods

We retrospectively evaluated 368 patients who performed 18F-choline-PET/CT between June 2016 and August 2018. The PET images were analyzed visually and semi-quantitatively by measuring the maximum standardized uptake value (SUVmax) and the mean SUV (SUVmean) of the thyroid gland and of the FTIU; every focal thyroid uptake deviating from physiological distribution and background was considered FTIU. Final diagnosis of FTIU was obtained by cytological or histological examination after surgery.

Results

The average SUVmax and SUVmean of thyroid gland in population were 3 and 1.8. Among 368 patients, FTIU was identified in nine cases (2.4%) and eight underwent further investigations to determine the nature. Two FTIU were classified as malignant (thyroid carcinoma), whereas five were benign (three nodular hyperplasia, one follicular adenoma, one Hurtle cell adenoma) and one indeterminate at cytological examination. In malignant lesions, average SUVmax was 9.6 and 4.5, respectively, while average SUVmean was 5.3 and 2.9, respectively. Average SUVmax and SUVmean of benign lesions were 4.9 and 3.2 and of the indeterminate lesion 5 and 3, respectively.

Conclusions

18F-choline-PET/CT FTIU may be a relevant diagnostic reality, which requires further investigations and affects management, especially considering that, despite being mainly benign, also malignancy is possible.



http://bit.ly/2ETjhPI

Ichthyosiform sarcoidosis: a mimic of leprosy?



http://bit.ly/2Va7FgW

Lupus erythematosus profundus in a patient with dermatomyositis



http://bit.ly/2QaHjrm

Sex‐related differences of clinical features in hidradenitis suppurativa: analysis of an Italian‐based cohort

Summary

The clinical characteristics associated with hidradenitis suppurativa (HS) severity are poorly understood. In this study, 124 patients with HS from 6 Italian dermatology centres participated in this study. Disease severity was assessed using the Hidradenitis Suppurativa Physician's Global Assessment score (HS‐PGA) and Hurley score. The impact of clinical characteristics on disease severity was assessed by logistic regression. Clinical characteristics were similar between men (n = 53) and women (n = 71). Disease severity was also similar; 75% of the patients had Hurley stage II or III disease, and > 60% had moderate, severe or very severe HS as judged by HS‐PGA. Lesions were more frequent in the gluteal region in men (32.3% in men vs. 8.7% in women, P < 0.001) and more frequent on the breast in women (16.3% in women vs. 4.6% in men, P = 0.02). Obesity was associated with increased disease severity as measured by HS‐PGA (OR: 3.28, 95% CI 1.55–6.95, P < 0.01) and Hurley classification (OR: 3.22, 95% CI 1.34–7.31, P < 0.01). Although severity of HS is similar between the sexes, the localization of lesions is different.



http://bit.ly/2ViVdMa

BRAF‐positive Multifocal and Unifocal Papillary Thyroid Cancer Show Different mRNA Expressions

Summary

Objective

Thyroid cancer is the most common malignant endocrine tumor, and its incidence has continuously increased worldwide over the past three decades. We focused on the association of multifocal PTC with mRNA expression to characterize how molecular and histopathologic features relate to multifocality.

Design

A retrospective cohort study.

Patients

The primary and processed data were downloaded from The Cancer Genome Atlas. Total 490 patients were included in this study.

Methods

The statistical significance of differences in sex, age, histology, LN metastasis, and recurrence were analyzed using chi‐squared test. To identify differentially expressed genes between BRAF (+) multifocal and unifocal PTCs and between BRAF (‐) multifocal and unifocal PTCs, we used the Significance Analysis of Microarray. Over‐representation analysis is conducted using CPDB.

Results

237 patients had BRAF (+) PTCs, whereas 253 had BRAF (‐) PTCs. There were 110 patients with multifocal PTCs and 127 with unifocal PTCs in the BRAF (+) group and 116 patients with multifocal PTCs and 137 with unifocal PTCs in the BRAF (‐) group. In BRAF (+) group, multifocal PTCs had increased expression of 158 mRNAs as compared to that in unifocal PTCs. 10 mRNAs were involved in Wnt‐related pathways and 7 mRNAs were included in pluripotency‐related pathways.

Conclusion

Multifocal PTCs have higher expression of mRNAs in Wnt‐ and pluripotency‐related pathways when BRAF mutation is present. This might be the mechanism that accounts for the difference between multifocal and unifocal PTCs.

This article is protected by copyright. All rights reserved.



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Violaceous Papules Presenting on the Foot and Lower Limb: Challenge

No abstract available

http://bit.ly/2ViOMZw

Localized Lichen Myxedematosus With Plasma Cell Light Chain Restriction. Is It the Exception or the Rule?

Lichen myxedematosus is a chronic cutaneous mucinosis that can present on a spectrum from localized cutaneous lesions to systemic disease of scleromyxedema. The clinical presentation of localized cutaneous lichen myxedematosus is waxy lichenoid papules, nodules, and/or plaques that have histopathologic findings of mucin deposition and a variable degree of fibroblast proliferation. There is an absence of serum paraproteins, and there are no other systemic causes of cutaneous mucinosis such as thyroid disease. The pathogenesis of lichen myxedematosus is unknown. We report 3 cases of localized cutaneous lichen myxedematosus with a light chain–restricted plasmacytic component by in situ hybridization. Our findings deliver an insight for disease pathogenesis and highlight for the first time, the significance of plasma cells in lesions of localized cutaneous lichen myxedematosus. We suggest that plasma cell light chain restriction could represent a clue to distinguish localized cutaneous disease from systemic disease. Correspondence: Laszlo Karai, MD, PhD, 16250 NW 59th Avenue, Miami Lakes, FL 33014 (e-mail: lkarai@auroradx.com). The authors declare no conflicts of interest. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

http://bit.ly/2Q8NEUq

Cutaneous B-Cell Lymphoblastic Lymphoma

Abstract: B-cell lymphoblastic lymphoma (B-LBL) is a malignant neoplasm of immature B cells that accounts for only 10% of all cases of lymphoblastic lymphoma. Most commonly, B-LBL presents as bony lesions, but in rare cases, the disease manifests cutaneously. We present a case of simultaneous cutaneous and systemic presentation of B-LBL in an otherwise healthy 28-year-old man in which the lymphoblastic infiltrate stained positive for CD79a, Tdt, CD10, and CD20. A diagnosis of cutaneous B-LBL was made, and systemic work-up revealed widespread involvement of the skin, bone, and lymph nodes. Review of all currently described cases of cutaneous B-LBL with or without systemic involvement revealed that the most frequently positive tumor markers were CD79a (92.3%), Tdt (90.6%), and CD10 (83.3%). Systemic involvement of B-LBL was found in nearly half of all cases with cutaneous presentation. Correspondence: Dilru Amarasekera, MD, Sidney Kimmel Medical College, Thomas Jefferson University, 1025 Walnut Street, Philadelphia, PA 19107 (e-mail: dca008@jefferson.edu). The authors declare no conflicts of interest. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

http://bit.ly/2VjZgI7

Granulomatous Reaction to Intralesional Kenalog (Triamcinolone) Injection in Acne: a Case Report

Abstract: Intralesional Kenalog (triamcinolone) injection is a useful treatment for several skin conditions. Although dermal deposition of triamcinolone has been described in the literature, histopathologic findings of foreign body reactions to it have seldom been reported. Here, we describe a case of a granulomatous reaction to the intralesional injection of triamcinolone acetonide in the treatment of nodulocystic acne. Correspondence: Ying Guo, MD, Ackerman Academy of Dermatopathology, 145 East 32nd Street, 10th Floor, New York, NY 10016 (e-mail: yguo@dermpathdiagnostics.com). The authors declare no conflicts of interest. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

http://bit.ly/2Q8NrRd

BRAF Inhibitor–Associated Granulomatous Dermatitis: A Report of 3 Cases

Abstract: Cutaneous toxicities associated with BRAF inhibitor treatment in patients with metastatic melanoma have been well described. We present a rare association of granulomatous dermatitis in association with the BRAF inhibitor vemurafenib. Three patients with metastatic melanoma all presented with asymptomatic papular eruptions 8–21 months into vemurafenib therapy. Skin biopsies confirmed the diagnosis of granulomatous dermatitis. Other causes of granulomatous dermatitis including infectious agents and sarcoid were excluded. Treatment with potent topical and oral steroids improved the eruptions, but only after the cessation of vemurafenib did all 3 cases of granulomatous dermatitis completely resolve within 2 weeks. It is important to recognize that this association, unlike most other BRAF inhibitor–related skin toxicities, can occur many months after commencement of therapy and that vemurafenib treatment can be continued without clinically significant adverse effects. Correspondence: Shilan Jmor, MBChB, Oncology Department, University College Hospital London, 235 Euston Road, London NW1 2BU (e-mail: shilanjmor@nhs.net). The authors declare no conflicts of interest. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

http://bit.ly/2VjZ23J

Superficial and Deep Cutaneous Involvement by RAS-Associated Autoimmunne Leukoproliferative Disease (RALD Cutis): A Histologic Mimicker of Histiocytoid Sweet Syndrome

Abstract: RAS-associated autoimmune leukoproliferative disease (RALD) is a recently described noninfectious and nonmalignant clinical syndrome characterized by autoimmune disorders, massive splenomegaly, modest lymphadenopathy, and monocytosis. On the molecular level, RALD is defined by somatic mutations of either NRAS or KRAS gene in a subset of hematopoietic cells. To date, there is a dearth of well-documented histopathologic description of cutaneous involvement by RALD in the literature. In the current case report, a 43-year-old female patient with a history of RALD presented with clinical pictures of sepsis and an erythematous rash in the left lower extremity. Histologic examination revealed a dense perivascular and interstitial infiltrate of immature myeloid cells admixed with scattered neutrophils involving the dermis and subcutaneous adipose tissue, imparting a panniculitis-like histologic pictures. There was a strong angiocentric propensity of the immature hematopoietic cells as well as extensive extravasation of red blood cells, even in the subcutaneous adipose tissue. Immunohistochemically, the immature hematopoietic cells were positive for CD43, CD4, and CD68, but negative for CD34, CD117, and myeloperoxidase. Overall, the histologic and cytologic findings were highly reminiscent of histiocytoid Sweet syndrome. Review of the English literature revealed cutaneous involvements by RALD only in patients with KRAS mutation compared with none of its NRAS counterparts. However, larger clinicopathologic studies on cutaneous involvement by RALD are warranted. The term "RALD cutis" with its histologic and molecular features is suggested to serve as a potential groundwork for future studies of this rare phenomenon. Correspondence: Tien Anh N. Tran, MD, Department of Pathology, Florida Hospital Orlando, 601 East Rollins Street, Orlando, FL 32803 (e-mail: tien.tran.md@flhosp.org). The authors declare no conflicts of interest. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

http://bit.ly/2Q7B33S

Comparison of the Inflammatory Infiltrates in Tumoral Melanosis, Regressing Nevi, and Regressing Melanoma

Background: Tumoral melanosis (TM) is a histologic diagnosis characterized by abundant pigment-laden macrophages in the dermis. It is generally thought to represent a regressed melanoma, although it has also been reported after benign pigmented lesions as well. Determining the antecedent lesion in cases of TM is of clinical importance to accurately guide therapy and prognostication. Comparing the histopathologic and immunohistochemical (IHC) characteristics of TM, halo nevi (HN), and regressing melanoma (RM) may help predict the antecedent lesion in cases of TM. Methods: Cases of TM, HN, and RM were selected and assessed for histopathologic (preservation of junctional melanocytic component, depth and width, solar elastosis, fibrosis, and preservation of rete ridge architecture) and IHC (SOX-10, CD138, and PD-1) parameters. PD-L1 immunostaining was also evaluated in cases of HN and RM. Results: Severe solar elastosis, fibrosis, and marked rete ridge effacement were more frequent in RM than in HN. By contrast, numerous plasma cells, clusters of lymphocytes expressing PD-1, and >50% PD-L1 expression in melanocytes were more common in HN than in RM. However, the association of these variables did not reach statistical significance. Discussion: Although studies with higher statistical power are needed, this study serves as an initial investigation to characterize the histopathologic and IHC characteristics, which may help better understand TM and its precursor lesions. Correspondence: Kiran Motaparthi, MD, Assistant Professor, Department of Dermatology, University of Florida College of Medicine, 4037 NW 86 Terrace, 4th Floor, Room 4130 Springhill, Gainesville, FL 32606 (e-mail: kmotaparthi@dermatology.med.ufl.edu). Financial support for this research was generously provided by the Franklin Flowers Melanoma Research Fund, University of Florida College of Medicine. Biostatistical analysis was performed in the Department of Biostatistics, University of Florida by Drs Susmita Datta, Alejandro Riveras Walker, and Dr Heather Lauritano. The authors declare no conflicts of interest. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

http://bit.ly/2VjYNWn

Dermoscopic and reflectance microscopy features of primary and metastatic Merkel cell carcinoma: Ten cases



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Atypical Asphysia

http://www.jfsmonline.com/article.asp?issn=2349-5014;year=2018;volume=4;issue=4;spage=233;epage=237;aulast=Cao

Forensic investigation of atypical asphysia


1 Anshan Public Security Bureau, Anshan, China
2 Key Laboratory of Evidence Science (China University of Political Science and Law), Ministry of Education, China, Collaborative Innovation Center of Judicial Civilization, China
3 Key Laboratory of Evidence Science (China University of Political Science and Law), Ministry of Education, China, Collaborative Innovation Center of Judicial Civilization; Key Laboratory of Forensic Genetics of Ministry of Public Security, Institute of Forensic Science, Ministry of Public Security, Beijing, China


Correspondence Address:
Dr. Dong Zhao
25 Xitucheng Road, Haidian, Beijing 100088 
China

  Abstract 


Smothering, choking, confined spaces, traumatic asphyxia, positional asphyxia, and other kinds of atypical mechanical asphyxia are not rare in forensic practice. However, these are not commonly well demonstrated in forensic monographs worldwide. The authors researched related works and literatures and summarized these with a view to contribute to the existing teaching resources and provide help to forensic practitioners who are involved in scene investigation and identification of such deaths.

Keywords: Asphyxia, forensic pathology, forensic medicine




  Introduction Top


Death caused by compression of the neck, such as from hanging, strangling, or throttling, is termed "mechanical asphyxia" and usually has obvious physical findings. However, asphyxias that result from no direct pressure on the neck vessels or trachea, lack typical morphological changes, or result in minimal damage are called "subtle asphyxias"[1] or "atypical mechanical asphyxias," used in this article. Atypical mechanical asphyxias include smothering, choking, environmental hypoxia, traumatic asphyxia, and positional asphyxia, among others.


  Smothering Top


Smothering is a form of asphyxia death caused by obstructing the mouth and nose with hands, airtight papers, soft textiles, or the weight of one's own head.[2]

Smothering can be seen in homicidal or suicidal cases. Homicidal smothering is common in infants, older adults, and people who are unconscious or have restricted motion due to fabric bundling, disease, poisoning, or intoxication. Homicidal smothering can also result when there are significant physical power differences between a perpetrator and victim.[3],[4],[5] Suicidal smothering is common in psychiatric patients; an example includes wrapping tape around one's mouth, nose, or the entire face.[6] Smothering can also occur accidentally. For example, adults who are unconscious or paralyzed because of drunkenness, epilepsy, drug overdose, or having another disease might accidentally asphyxiate themselves. Similarly, for an infant lying face down on an airtight mattress or pillow, the weight of the infant's head might obstruct, distort, and occlude his or her mouth and nose, leading to suffocation. In a third example, sleeping infants with clothes or bedding covering their faces are at an increased risk of suffocation.[1],[2]

In general, it is difficult to identify a case of smothering during forensic scene examination because physical findings are nonspecific.[7],[8] If smothering is suspected, there may be local signs of pressure on the face.[2],[3] In adults, with even slight resistance, signs include skin exfoliation from fingernails; contusions on the nose, cheeks, or chin from fingers; bleeding and skin tears corresponding to the teeth in the oral mucosa; and intramuscular bleeding at the mandibular margin. Nasal deformation is also considered a sign of smothering, but can be caused by emergency tracheal intubation.[3],[5],[7] In infants and adults who are unable to physically resist during asphyxiation, physical damage is difficult to detect.[3] Of note, a body in the prone position concentrates pressure on the face, preventing accumulation of blood into the compressed skin around the mouth and nose, leading to the formation of distinct pale areas caused by the absence of pooled blood. It is, therefore, important not to assume that pale areas such as these have resulted from indentation by smothering.[2]

Without positive physical findings in smothering cases, scene investigation plays a decisive role. Pillows and bedding should be examined for blood or lipstick.[5],[9] For suspected cases of smothering, even if postmortem changes are obvious, suspicious skin lesions should be biopsied for histological examination.[5] In cases of smothering by textiles, the mouth, nasal cavity, and airways should be examined for inhaled fabric fibers. Fibers in the trachea indicate that a patient may have been alive during smothering.[8]

Gagging generally involves placing fabric in a victim's mouth to prevent yelling; the fabric gradually becomes soaked with saliva, and if airtight, will lead to suffocation. Another form of gagging involves placing tape over the mouth or nose, which results in trapped mucus production that eventually leads to suffocation. Obstruction of the nasopharynx by objects in the oral cavity may also lead to gagging and subsequent death.[2] Usually, suspected gagging is confirmed when blocking objects are found, not by any specific physical signs of asphyxia.[3]


  Choking Top


Choking refers to upper respiratory tract blockage by a foreign body leading to suffocation. The foreign body is usually lodged between the larynx and trachea.[10],[11] Death may result from simple hypoxia; however, many deaths occur quickly before the onset of hypoxia. Studies have found that, even in cases in which the airway is not completely blocked, death often occurs, likely from neurogenic-induced cardiac arrest.[2],[9],[11],[12]

Choking is almost always accidental, with cases of homicide and suicide relatively rare.[1],[11] For infants, accidental choking most often occurs with foreign body ingestion; for adults, choking most often occurs with food.[1],[11] Victims in homicidal choking cases are most likely to be older adults, infants, young children, people who are unconscious, or persons debilitated by illness or intoxication. Suicidal choking most often occurs in patients with psychosis or prisoners in jail.[1]

Evidence of coughing helps eliminate choking as a cause of death because it signifies that the respiratory tract was open during upper respiratory blockage.[3] Computed tomography imaging can provide information before an autopsy on the location of a foreign body and can help inform an autopsy plan.[13] Few physical findings are generally seen in choking deaths, so the discovery of a foreign body in the airway, a detailed clinical history, descriptions of the death environment and any resuscitation attempts, and exclusion of other causes of death are critical when forming a conclusion.[1],[9],[11],[12] If the foreign body shifts during resuscitation or otherwise is moved, clinical history might be the only evidence.[3],[13]

Foreign bodies blocking the airway leading to choking generally belong to the following categories.[2]

Foreign objects

Attackers may put a towel or sock into the victim's mouth to prevent shouting; this can cause choking and gagging.[3] In another example, people may inhale sand, piles of gravel, or piles of soil when they fall on them, causing respiratory blockage and resulting in choking death. This scenario may occur accidentally at a construction site, during a traffic accident, or in children playing in or eating sand.[3],[14]

Acute obstruction

Acute allergy, steam stimulation, heat inhalation, and acute inflammation may cause swelling of the throat organs, including the epiglottis, tonsils, or glottis, leading to choking. Trauma in the anterior or lateral cervical neck structures can also result in severe swelling of the respiratory tract from bleeding and edema.[1],[2],[7] Tumors, polyps, or cysts can also block respiration, leading to choking.[1],[10],[11]

Foods

The most common foreign bodies causing choking death in adults are foods.[10] Susceptible factors include old age, neuromuscular disease, poor dentition leading to chewing problems, consumption of alcohol or other central nervous system depressants weakening the gag reflex, or other neurological or mental illness (of which poor dentition is an important risk factor).[1],[11],[12],[13] Of patients with mental illness, those with schizophrenia are most likely to choke on food, possibly from a propensity to swallow incompletely chewed food.[11] The majority of adult choking cases occur at patients' homes, nursing homes, or mental hospitals, and often take place suddenly during meals.[1]

When a sudden death occurs while eating or soon after, the possibility of choking must be considered. A search for a blocked airway should be initiated, but in addition, the investigator should also consider factors that could have aggravated the choking episode. Therefore, quality and number of teeth, food debris in the esophagus – which can cause tracheal obstruction from the external oppression – and exclusion of neurological diseases and intoxication are all important when evaluating sudden death during a meal.[1],[9],[11],[12]

It is typical for gastric contents to be present in the throat, trachea, and bronchi after death, caused by reflux or shifting of contents. This is a common postmortem phenomenon, found in 20%–25% of routine examinations. As a result, if a small amount of gastric content is found in the respiratory tract, this does not mean that choking had occurred; however, if the throat or airway is completely blocked by gastric contents, choking can be concluded.[2],[3],[13] The inhalation of gastric contents is more common in people who are unconscious.[1]Importantly, there is no reliable way to distinguish natural food reflux early in the dying process from true inhalation while alive, unless the inhalation occurred during a clinical procedure or another person witnessed the event. In most cases, in the absence of hard evidence, it is unreasonable for forensic officers to conclude that the inhalation of gastric contents is secondary to choking death.[2]


  Environmental Hypoxia Top


Environmental asphyxiation is usually caused by a lack of oxygen in the local environment,[1],[2],[3] and is almost always accidental. Oxygen deficiency can occur secondary to breathing exercises, microbial consumption, activities related to industrial work (such as welding), environmental chemical reactions (such as rust), absorption by chemical substances (such as activated carbon), and presence of toxic gases (such as propane, nitrogen, and methane).[1],[2],[3] An atmospheric oxygen concentration below 5%–10% will cause death in a few minutes, and a concentration of carbon dioxide higher than 10% is lethal.[1] In some cases, death occurs before the onset of hypoxia, and is secondary to overexcitement of the body's chemical sensing system, which causes parasympathetic nervous system-mediated cardiac arrest.[2]

In hypoxia-asphyxia deaths caused by low atmospheric oxygen levels, physical findings are usually absent,[2] making elucidation of the specific cause of death difficult. Investigators must carefully analyze the environment and exclude other causes of death to conclude environmental hypoxia-asphyxia.[3] Measurements of toxic gases and oxygen concentrations in the air, as well as postmortem analysis of blood and tissues, should be performed; in addition, scene simulations may be required.[1]

As a type of environmental hypoxia-asphyxia, plastic bag suffocation is often used as a suicide technique in Western countries. This method is common in young men and elderly women.[15] Some people even use the propane, ether, or helium gas along with the plastic bag. Plastic bag suffocation deaths can also occur accidentally or unexpectedly, such as during sexual asphyxia, children playing with plastic bags, and other occurrences.[1] It is very rare for the use of plastic bags to result in death; however, it is more likely in cases in which the victim is unconscious, or when there is a large difference in strength between the perpetrator and victim.[16]

Plastic bag suffocation often occurs rapidly with few physical signs;[1],[2] however, in a small number of cases, marks on the neck are present corresponding to the areas of bag bundling (such as from a rubber band), or there may be signs of prior injury, such as wrist cutting or abuse.[1],[2] It is a common misconception that the postmortem presence of moisture in the plastic bag confirms that the bag was placed on a breathing human; water droplets form as gas evaporates from the skin, nose, and mouth even if the person was previously deceased.[2]

Because there are usually no specific physical findings, it is difficult to identify cases of plastic bag suffocation unless the bag is over the head at the time of scene investigation or autopsy.[2] If the plastic bag is removed before forensic workers see the corpse, they will not be able to determine the cause of death through forensic examination, and may even conclude that a natural death occurred. Therefore, to identify such cases, forensic workers must pay careful attention during scene exploration and investigation.[1],[3],[9],[16] If necessary, forensic workers can conduct simulations under close monitoring in a protected environment, which can help to pinpoint a cause of death through analysis of time measurements.[4],[6],[17] Specimens collected from the blood, lungs, liver, or other organs for poison analysis should be extracted and stored in a sealed empty bottle along with a plastic bag,[2],[7],[16] frozen, and delivered promptly.[1]


  Traumatic Asphyxia Top


Traumatic asphyxia refers to the compression of the chest or abdomen by massive mechanical forces resulting in thoracic fixation – expansion of thoracic and lower phrenic muscles – leading to respiratory disturbance and death by asphyxiation.[2]

Traumatic asphyxia is common in the following types of accidents: motor vehicle compression or extrusion during traffic accidents; pinning from building collapse, falling rocks, or other objects; trampling by a crowd; compression while standing in a crowded population from sudden external forces; compression by fallen tools or furniture; and compression of infants and children while sleeping with parents (overlaying asphyxia).[1],[2],[18] There are also reports of homicide resulting from a perpetrator kneeling or sitting on the chest of a victim.[19]

The pathological features of traumatic asphyxia are usually quite specific. These include prominent facial and nuchal hyperemia and swelling; numerous petechial hemorrhages on the face or conjunctiva; subconjunctival hemorrhage and edema; and nasal bleeding. In general, a person who dies from traumatic asphyxiation often appears strangled with features extending down to the neck, with no signs of local damage.[2],[20],[21]

However, physical features such as these are not always visible. Studies have shown that, in up to 10% of cases, no petechial hemorrhages are seen on the face or conjunctiva. The reason for this is unclear, but may be related to rapidness of death, lack of obvious chest compression or vagus nerve stimulation, lack of occlusion of the epiglottis, or concurrence of both left heart and right heart impairment at the time of chest compression.[1],[18],[20],[21] On gross examination, lungs may have a purplish red color, congestion, or subserous bleeding with or without obvious expansion of the right heart or superior vena cava; sometimes, there is no evidence of trauma despite severe direct external compression on the chest and abdomen.[1],[2],[3],[9]

Traumatic asphyxia is a diagnosis of exclusion. In addition to supporting evidence from a scene investigation, suffocation death should only be considered after excluding fatal injuries and poisoning.[1],[9],[21]

Overlaying asphyxia is a special form of traumatic asphyxia, often secondary to nasal compression. Physical examination findings are usually absent, so overlaying can be difficult to determine unless the same-bed sleeper admits to crushing the infant or child. Overlaying asphyxia is sometimes attributed to sudden infant death syndrome, so it is important to examine adults' and children's clothes and bedding carefully as well as the scene.[1],[3],[22]


  Positional Asphyxia Top


Positional asphyxia refers occurrences in which respiration is compromised from splinting of the chest or diaphragm preventing normal respiration, or occlusion of the upper airway due to abnormal positioning of the body.[23] Positional asphyxia is almost always an accident, during which the victim cannot extract himself or herself from a specific position or small space. The victim may be further impaired by alcohol or drug intoxication, weakness, neurological disease, or fabric bundling. Common examples of positional asphyxia include limbs tied behind the back while in a prone position (may be performed for restraint by police or psychiatrists for suspects or patients); head-down position (inversion of the body, or head hanging down off the edge of a bathtub); jack-knife position (upper body significantly curved from the waist down); bundled thoracic or abdominal horizontal sling (e.g., a young girl wearing a belt hanging by the abdomen on a swing); excessive flexion or extension of the neck (e.g., during a motor vehicle accident); lack of chest wall expansion in a restricted space (wedging); and a person sandwiched between the wall and the mattress after falling off the bed.[1],[2],[3],[4],[5],[6],[7],[24] A typical case of postural asphyxia involves a drunken person who collapses into a narrow space, excessively distorting the neck and hindering breathing, leading to death.[9]

Cause of death from positional asphyxia often results from reverse suspension of the body such that the movement of the chest wall is restricted by intra-abdominal organs compressing the diaphragm. This prolongs inspiration, and eventually results in respiratory muscle fatigue, leading to slowed movement of the chest wall and subsequent hypoxia. Venous return is effectively limited, and blood flow to the brain is shifted, decreasing blood flow and further aggravating respiratory muscle fatigue; eventually, the heart stops.[1] Positional asphyxia does not require reversal of the entire body; fatal asphyxia may result from the reversal of torso position, excessive flexion of the neck, or pressure on one's face, such as in an intoxicated person whose face is pressed to the floor.[25] The difference between traumatic asphyxia and positional asphyxia is whether the chest and abdomen are compressed by external forces. If chest compression is from an external source, he or she should have been died from traumatic asphyxia. If a deceased person is found in a specific position or restricted space that limits chest activity, the person should have been died from positional asphyxia.[1],[23]

Positional asphyxia can be identified by the following criteria: The body position is consistent with restricted or disordered respiration; scene investigation or historical investigation identifies that an accident had occurred; the deceased person cannot change his or her position for some reason; and other obvious natural or violent causes of death are excluded. A diagnosis of accidental positional asphyxia mainly depends on the evidence obtained from the scene environment.[24],[25] Some forensic investigators believe that, if another disease is present, then either the cause of death is not associated with positional asphyxia, or the onset of the disease makes the deceased patient prone to positional asphyxia.[23] It should be noted that alcohol consumed by a patient with positional asphyxia may be metabolized. Thus, even if the concentration of alcohol in the blood or urine is very low or negative, the possibility of positional asphyxia cannot be ignored.[24]

Wedging is a special form of positional asphyxia, commonly seen in infants and young children whose body or head are compressed in a narrow space. The chest wall is fixed, resulting in airway obstruction that results in asphyxia. Wedging usually occurs between a mattress and wall or mattress and furniture or baby crib. It is most common in infants aged 3–6 months, intoxicated adults, or comatose patients who accidentally fall between a mattress and wall, leading to death. Physical findings of wedging are usually absent.[1],[22]

Acknowledgments

This study was supported by the Open Project of Key Laboratory of Forensic Genetics, Ministry of Public Security (2017FGKFKT05), Program for Young Innovative Research Team from China University of Political Science and Law (2016CXTD05), and Project of Interdisciplinary Science Construction-Forensic Psychology from China University of Political Science and Law.  

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