Forensic Lung Pathology
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Forensic Medicine
YEREVAN STATE MEDICAL UNIVERSITY AFTER M. HERATSI DEPARTMENT OF Sh. Vardanyan K. Avagyan S. Hakobyan FORENSIC MEDICINE Handout for foreign students YEREVAN 2007 This handbook is adopted by the Methodical Council of Foreign Students of the University DEATH AND ITS CAUSES Thanatology deals with death in all its aspects. Death is of two types: (1) somatic, systemic or clinical, and (2) molecular or cellular. Somatic Death: It is the complete and irreversible stoppage of the circulation, respiration and brain functions, but there is no legal definition of death. THE MOMENT OF DEATH: Historically (medically and legally), the concept of death was that of "heart and respiration death", i.e. stoppage of spontaneous heart and breathing functions. Heart-lung bypass machines, mechanical respirators, and other devices, however have changed this medically in favor of a new concept "brain death", that is, irreversible loss of Cerebral function. Brain death is of three types: (1) Cortical or cerebral death with an intact brain stem. This produces a vegetative state in which respiration continues, but there is total loss of power of perception by the senses. This state of deep coma can be produced by cerebral hypoxia, toxic conditions or widespread brain injury. (2) Brain stem death, where the cerebrum may be intact, though cut off functionally by the stem lesion. The loss of the vital centers that control respiration, and of the ascending reticular activating system that sustains consciousness, cause the victim to be irreversibly comatose and incapable of spontaneous breathing. This can be produced by raised intracranial pressure, cerebral oedema, intracranial haemorrhage, etc.(3) Whole brain death (combination of 1 and 2). -
USMLE – What's It
Purpose of this handout Congratulations on making it to Year 2 of medical school! You are that much closer to having your Doctor of Medicine degree. If you want to PRACTICE medicine, however, you have to be licensed, and in order to be licensed you must first pass all four United States Medical Licensing Exams. This book is intended as a starting point in your preparation for getting past the first hurdle, Step 1. It contains study tips, suggestions, resources, and advice. Please remember, however, that no single approach to studying is right for everyone. USMLE – What is it for? In order to become a licensed physician in the United States, individuals must pass a series of examinations conducted by the National Board of Medical Examiners (NBME). These examinations are the United States Medical Licensing Examinations, or USMLE. Currently there are four separate exams which must be passed in order to be eligible for medical licensure: Step 1, usually taken after the completion of the second year of medical school; Step 2 Clinical Knowledge (CK), this is usually taken by December 31st of Year 4 Step 2 Clinical Skills (CS), this is usually be taken by December 31st of Year 4 Step 3, typically taken during the first (intern) year of post graduate training. Requirements other than passing all of the above mentioned steps for licensure in each state are set by each state’s medical licensing board. For example, each state board determines the maximum number of times that a person may take each Step exam and still remain eligible for licensure. -
Aspiration Pneumonia and Related Syndromes
REVIEW Aspiration Pneumonia and Related Syndromes Augustine S. Lee, MD, and Jay H. Ryu, MD Abstract Aspiration is a syndrome with variable respiratory manifestations that span acute, life-threatening illnesses, such as acute respiratory distress syndrome, to chronic, sometimes insidious, respiratory disorders such as aspiration bronchiolitis. Diagnostic testing is limited by the insensitivity of histologic testing, and although gastric biomarkers for aspiration are increasingly available, none have been clinically validated. The leading mechanism for microaspiration is thought to be gastroesophageal reflux disease, largely driven by the increased prevalence of gastroesophageal reflux across a variety of respiratory disorders, including chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, and chronic cough. Failure of therapies targeting gastric acidity in clinical trials, in addition to increasing concerns about both the overuse of and adverse events associated with proton pump inhibitors, raise questions about the precise mechanism and causal link between gastroesophageal reflux and respiratory disease. Our review summarizes key aspiration syndromes with a focus on reflux-mediated aspiration and highlights the need for additional mechanistic studies to find more effective therapies for aspiration syndromes. ª 2018 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2018;nn(n):1-11 ulmonary aspiration is the pathologic pas- unchallenged with empirical attempts at moder- From the Division of fl Pulmonary, -
Heat Stroke Heat Exhaustion
Environmental Injuries Co lin G. Ka ide, MD , FACEP, FAAEM, UHM Associate Professor of Emergency Medicine Board-Certified Specialist in Hyperbaric Medicine Specialist in Wound Care The Ohio State University Wexner Medical Center The Most Dangerous Drug Combination… Accidental Testosterone Hypothermia and Alcohol! The most likely victims… Photo: Ralf Roletschek 1 Definition of Blizzard Hypothermia of Subnormal T° when the body is unable to generate sufficient heat to sustain normal functions Core Temperature < 95°F 1979 (35°C) Most Important Temperatures Thermoregulation 95°F (35° C) Hyper/Goofy The body uses a Poikilothermic shell to maintain a Homeothermic core 90°F (32°C) Shivering Stops Maintains core T° w/in 1.8°F(1°C) 80°F (26. 5°C) Vfib, Coma Hypothalamus Skin 65°F (18°C) Asystole Constant T° 96.896.8-- 100.4° F 2 Thermoregulation The 2 most important factors Only 3 Causes! Shivering (10x increase) Decreased Heat Production Initiated by low skin temperature Increased Heat Loss Warming the skin can abolish Impaired Thermoregulation shivering! Peripheral vasoconstriction Sequesters heat Predisposing Predisposing Factors Factors Decreased Production Increased Loss –Endocrine problems Radiation Evaporation • Thyroid Conduction* • Adrenal Axis Convection** –Malnutrition *Depends on conducting material **Depends on wind velocity –Neuromuscular disease 3 Predisposing Systemic Responses CNS Factors T°< 90°F (34°C) Impaired Regulation Hyperactivity, excitability, recklessness CNS injury T°< 80°F (27°C) Hypothalamic injuries Loss of voluntary -
Environmental Injuries
Environmental Injuries Colin G. Kaide, MD, FACEP, FAAEM, UHM Associate Professor of Emergency Medicine Board-Certified Specialist in Hyperbaric Medicine Specialist in Wound Care The Ohio State University Wexner Medical Center 1 The Most Dangerous Drug Combination… Testosterone and Alcohol! The most likely victims… Photo: Ralf Roletschek Accidental Hypothermia 2 Blizzard of 1979 Definition of Hypothermia Subnormal T° when the body is unable to generate sufficient heat to sustain normal functions Core Temperature < 95°F (35°C) 3 Most Important Temperatures 95°F (35° C) Hyper/Goofy 90°F (32°C) Shivering Stops 80°F (26.5°C) Vfib, Coma 65°F(18F (18°C) AtlAsystole Thermoregulation The body uses a Poikilothermic shell to maintain a Homeothermic core Maintains core T° w/in 1.8°F(1°C) Hypothalamus Skin CttTConstant T° 96. 8- 100.4° F 4 Thermoregulation The 2 most important factors Shivering (10x increase) Initiated by low skin temperature Warming the skin can abolish shivering! Peripheral vasoconstriction Sequesters heat Only 3 Causes! Decreased Heat Production Increased Heat Loss Impaired Thermoregulation 5 Predisposing Factors Decreased Production –Endocrine problems • Thyroid • Adrenal Axis –Malnutrition –Neuromuscular disease Predisposing Factors Increased Loss RRditiadiation Evaporation Conduction* Convection** *DDdepends on cond dtitilucting material **Depends on wind velocity 6 Predisposing Factors Impaired Regulation CNS injury Hypothalamic injuries Peripheral Injury Atherosclerosis Neuropathy Interfering Agents Systemic Responses CNS -
Venous Air Embolism, Result- Retrospective Study of Patients with Venous Or Arterial Ing in Prompt Hemodynamic Improvement
Ⅵ REVIEW ARTICLE David C. Warltier, M.D., Ph.D., Editor Anesthesiology 2007; 106:164–77 Copyright © 2006, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Diagnosis and Treatment of Vascular Air Embolism Marek A. Mirski, M.D., Ph.D.,* Abhijit Vijay Lele, M.D.,† Lunei Fitzsimmons, M.D.,† Thomas J. K. Toung, M.D.‡ exogenously delivered gas) from the operative field or This article has been selected for the Anesthesiology CME Program. After reading the article, go to http://www. other communication with the environment into the asahq.org/journal-cme to take the test and apply for Cate- venous or arterial vasculature, producing systemic ef- gory 1 credit. Complete instructions may be found in the fects. The true incidence of VAE may be never known, CME section at the back of this issue. much depending on the sensitivity of detection methods used during the procedure. In addition, many cases of Vascular air embolism is a potentially life-threatening event VAE are subclinical, resulting in no untoward outcome, that is now encountered routinely in the operating room and and thus go unreported. Historically, VAE is most often other patient care areas. The circumstances under which phy- associated with sitting position craniotomies (posterior sicians and nurses may encounter air embolism are no longer fossa). Although this surgical technique is a high-risk limited to neurosurgical procedures conducted in the “sitting procedure for air embolism, other recently described position” and occur in such diverse areas as the interventional radiology suite or laparoscopic surgical center. Advances in circumstances during both medical and surgical thera- monitoring devices coupled with an understanding of the peutics have further increased concern about this ad- pathophysiology of vascular air embolism will enable the phy- verse event. -
Traveler Information
Traveler Information QUICK LINKS Marine Hazards—TRAVELER INFORMATION • Introduction • Risk • Hazards of the Beach • Animals that Bite or Wound • Animals that Envenomate • Animals that are Poisonous to Eat • General Prevention Strategies Traveler Information MARINE HAZARDS INTRODUCTION Coastal waters around the world can be dangerous. Swimming, diving, snorkeling, wading, fishing, and beachcombing can pose hazards for the unwary marine visitor. The seas contain animals and plants that can bite, wound, or deliver venom or toxin with fangs, barbs, spines, or stinging cells. Injuries from stony coral and sea urchins and stings from jellyfish, fire coral, and sea anemones are common. Drowning can be caused by tides, strong currents, or rip tides; shark attacks; envenomation (e.g., box jellyfish, cone snails, blue-ringed octopus); or overconsumption of alcohol. Eating some types of potentially toxic fish and seafood may increase risk for seafood poisoning. RISK Risk depends on the type and location of activity, as well as the time of year, winds, currents, water temperature, and the prevalence of dangerous marine animals nearby. In general, tropical seas (especially the western Pacific Ocean) are more dangerous than temperate seas for the risk of injury and envenomation, which are common among seaside vacationers, snorkelers, swimmers, and scuba divers. Jellyfish stings are most common in warm oceans during the warmer months. The reef and the sandy sea bottom conceal many creatures with poisonous spines. The highly dangerous blue-ringed octopus and cone shells are found in rocky pools along the shore. Sea anemones and sea urchins are widely dispersed. Sea snakes are highly venomous but rarely bite. -
An Atypical Case of Recurrent Cellulitis/Lymphangitis in a Dutch Warmblood Horse Treated by Surgical Intervention A
EQUINE VETERINARY EDUCATION / AE / JANUARY 2013 23 Case Report An atypical case of recurrent cellulitis/lymphangitis in a Dutch Warmblood horse treated by surgical intervention A. M. Oomen*, M. Moleman, A. J. M. van den Belt† and H. Brommer Department of Equine Sciences and †Companion Animals, Division of Diagnostic Imaging, Faculty of Veterinary Medicine, Utrecht University, Yalelaan, Utrecht, The Netherlands. *Corresponding author email: [email protected] Keywords: horse; lymphangitis; lymphoedema; surgery; lymphangiectasia Summary proposed as a possible contributing factor for chronic The case reported here describes an atypical presentation progressive lymphoedema of the limb in these breeds of of cellulitis/lymphangitis in an 8-year-old Dutch Warmblood horses (de Cock et al. 2003, 2006; Ferraro 2003; van mare. The horse was presented with a history of recurrent Brantegem et al. 2007). episodes of cellulitis/lymphangitis and the presence of Other diseases related to the lymphatic system are fluctuating cyst-like lesions on the left hindlimb. These lesions lymphangioma/lymphangiosarcoma and development appeared to be interconnected lymphangiectasias. Surgical of lymphangiectasia. Cutaneous lymphangioma has been debridement followed by primary wound closure and local described as a solitary mass on the limb, thigh or inguinal drainage was performed under general anaesthesia. Twelve region of horses without the typical signs of progressive months post surgery, no recurrence of cellulitis/lymphangitis lymphoedema (Turk et al. 1979; Gehlen and Wohlsein had occurred and the mare had returned to her former use as 2000; Junginger et al. 2010). Lymphangiectasias in horses a dressage horse. have been described in the intestinal wall of foals and horses with clinical signs of colic and diarrhoea (Milne et al. -
Asphyxia Neonatorum
CLINICAL REVIEW Asphyxia Neonatorum Raul C. Banagale, MD, and Steven M. Donn, MD Ann Arbor, Michigan Various biochemical and structural changes affecting the newborn’s well being develop as a result of perinatal asphyxia. Central nervous system ab normalities are frequent complications with high mortality and morbidity. Cardiac compromise may lead to dysrhythmias and cardiogenic shock. Coagulopathy in the form of disseminated intravascular coagulation or mas sive pulmonary hemorrhage are potentially lethal complications. Necrotizing enterocolitis, acute renal failure, and endocrine problems affecting fluid elec trolyte balance are likely to occur. Even the adrenal glands and pancreas are vulnerable to perinatal oxygen deprivation. The best form of management appears to be anticipation, early identification, and prevention of potential obstetrical-neonatal problems. Every effort should be made to carry out ef fective resuscitation measures on the depressed infant at the time of delivery. erinatal asphyxia produces a wide diversity of in molecules brought into the alveoli inadequately com Pjury in the newborn. Severe birth asphyxia, evi pensate for the uptake by the blood, causing decreases denced by Apgar scores of three or less at one minute, in alveolar oxygen pressure (P02), arterial P02 (Pa02) develops not only in the preterm but also in the term and arterial oxygen saturation. Correspondingly, arte and post-term infant. The knowledge encompassing rial carbon dioxide pressure (PaC02) rises because the the causes, detection, diagnosis, and management of insufficient ventilation cannot expel the volume of the clinical entities resulting from perinatal oxygen carbon dioxide that is added to the alveoli by the pul deprivation has been further enriched by investigators monary capillary blood. -
A Narrative Review of Minimally Invasive Fundoplication for Gastroesophageal Reflux Disease and Interstitial Lung Disease
7 Review Article Page 1 of 7 A narrative review of minimally invasive fundoplication for gastroesophageal reflux disease and interstitial lung disease Nicola Tamburini1, Ciro Andolfi2,3, P. Marco Fisichella4 1Department of Human Morphology, Surgery, and Experimental Medicine, Section of Chirurgia 1, University of Ferrara School of Medicine, Ferrara, Italy; 2Department of Surgery and Center for Simulation, The University of Chicago Pritzker School of Medicine and Biological Sciences Division, Chicago, IL, USA; 3MacLean Center for Clinical Medical Ethics, The University of Chicago, Chicago, IL, USA; 4Department of Surgery, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA Contributions: (I) Conception and design: All authors; (II) Administrative support: None; (III) Provision of study materials or patients: None; (IV) Collection and assembly of data: None; (V) Data analysis and interpretation: N Tamburini; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. Correspondence to: Nicola Tamburini. Department of Human Morphology, Surgery, and Experimental Medicine, Section of Chirurgia 1, University of Ferrara School of Medicine, Ferrara, Italy. Email: [email protected]. Abstract: Interstitial lung disease (ILD) encompasses a heterogeneous group of acute and chronic disorders characterized by diffuse pulmonary infiltrates with histologic features of pulmonary inflammation, dyspnea, and restrictive lung patterns. Gastroesophageal reflux disease (GERD) and ILD are two pathological conditions often strictly related, even if a clear relationship of causality has not been demonstrated. The mechanisms leading to ILD are not completely understood, although it is recognized that different factors are involved. In recent years, it has been suggested that acid gastroesophageal reflux is an important cause of both systemic sclerosis (SSc)-ILD and idiopathic pulmonary fibrosis (IPF). -
Lung Transplantation As Therapeutic Option in Acute Respiratory Distress Syndrome for Coronavirus Disease 2019-Related Pulmonary fibrosis
Original Article Lung transplantation as therapeutic option in acute respiratory distress syndrome for coronavirus disease 2019-related pulmonary fibrosis Jing-Yu Chen1, Kun Qiao2, Feng Liu1,BoWu1, Xin Xu3, Guo-Qing Jiao4, Rong-Guo Lu1, Hui-Xing Li1, Jin Zhao1, Jian Huang1, Yi Yang5, Xiao-Jie Lu6, Jia-Shu Li7, Shu-Yun Jiang8, Da-Peng Wang8, Chun-Xiao Hu9, Gui-Long Wang9, Dong-Xiao Huang9, Guo-Hui Jiao1, Dong Wei1, Shu-Gao Ye1, Jian-An Huang10, Li Zhou1, Xiao-Qin Zhang1, Jian-Xing He3 1Wuxi Lung Transplant Center, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi, Jiangsu 214023, China; 2Department of Thoracic Surgery, Shenzhen Third People’s Hospital, Shenzhen, Guangdong 518100, China; 3Department of Thoracic Surgery/Oncology, State Key Laboratory and National Clinical Research Center for Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510120, China; 4Department of Cardiothoracic Surgery, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi, Jiangsu 214023, China; 5Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu 210009, China; 6Wuxi Fifth Hospital, Wuxi, Jiangsu 214000, China; 7Department of Respiratory Medicine and Critical Care Medicine, The First People’s Hospital of Lianyungang City, Lianyungang, Jiangsu 222061, China; 8Department of Critical Care Medicine, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi, Jiangsu 214023, China; 9Department of Anesthesiology, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi, Jiangsu 214023, China; 10Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China. Abstract Background: Critical patients with the coronavirus disease 2019 (COVID-19), even those whose nucleic acid test results had turned negative and those receiving maximal medical support, have been noted to progress to irreversible fatal respiratory failure. -
Death & Decomposition Part II
Death & Decomposition Part II Review: Why is TSD/PMI so important? Review: What happens in the Fresh (1st) Stage of Decomposition? STAGE 2: Bloat ⦿ 0-10 days ⦿ Putrefaction: bacterially-induced destruction of soft tissue and gas formation › Skin blisters and marbling › Build-up of fluids from ruptured cells and intestines Putrefaction – the gross stuff ➢ Decomposition that occurs as a result of bacteria and other microorganisms ➢ Results in gradual dissolution of solid tissue into gases and liquids, and salts Putrefaction ➢ Characteristics: ○ Greenish discoloration ○ Darkening of the face ○ Bloating and formation of liquid or gas-filled blisters ○ Skin slippage Putrefaction ➢ Begins about 36 hours after death ➢ Further destruction is caused by maggots and insects ➢ Above 40 F, insects will feed until the body is skeletonized Influences of Putrefaction ➢ Heavy clothing and other coverings speed up the process by holding in body heat ➢ Injuries to the body surface promote putrefaction ○ provide portals of entry for bacteria Marbling Stage 3: Active Decay ➢ 10-20 days after death ➢ Body begins to collapse and black surfaces are exposed ➢ Bloated body collapses and leaves a flattened body ➢ Body fluids drain from body Active Decay Active Decay: Destruction of Tissue • Severe decomp can result in complete destruction of soft tissue Active Decay: Advanced Decomposition Stage 4: Dry Decay ➢ 20-365 days after death ➢ Remaining flesh on body is removed and body dries out ➢ Body is dry and continues to decay very slowly due to lack of moisture ➢