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Government works Printed in the United States of America on acid-free paper 10 9 8 7 6 5 4 3 2 1 International Standard Book Number: 978-1-4200-7836-7 (Hardback) This book contains information obtained from authentic and highly regarded sources discount fluconazole 200mg visa antifungal yeast treatment. Reasonable efforts have been made to publish reliable data and information discount fluconazole 50 mg fast delivery anti fungal wash for exterior walls, but the author and publisher cannot assume responsibility for the validity of all materials or the consequences of their use cheap fluconazole 200mg on-line antifungal tablet. The authors and publishers have attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained order fluconazole 150 mg otc fungus under toe. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. Copyright Law, no part of this book may be reprinted, reproduced, transmit- ted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-in-Publication Data Forensic dentistry / editors, David R. We also want to remember and salute that small group of concerned odon- tologists who met on Fire Island, New York, afer the impetus for the formation of various forensic boards was announced. Several others, including one editor and another contributor to this book, were invited to be included in the original group. Te board was incorporated in the District of Columbia with the frst certifcates awarded on February 18, 1976. Tis board has grown and developed and now includes dip- lomates from many American states and Canadian provinces. We are proud of the progress the board has made and its continu- ing support of educational and research eforts. We want to especially dedicate this book to each of you who hold it in your hands. If you are a forensic odontologist, you must strive to constantly improve the science and the feld, as did your mentors, with lectures, papers, and in person. In order for forensic odontology to progress to a specialty of dentistry there must be a consistent stream of new ideas and original and applied research. If you are not a forensic odontologist and are referring to this book, we welcome you to this challenging and fascinating feld. It is our hope that the material presented in this book will be, in some way, helpful to you for your inquiry. He was my student in pathology in dental school and has gone the extra mile for this second edition. His eforts are refected in the high caliber of the chapters in the book before you. Tis project would not have been possible without his hard work and vigorous encouragement to our contributors. Paul Stimson Table of Contents Preface ix The Editors xi The Contributors xiii 1 Science, the Law, and Forensic Identifcation 1 Christopher J. Golden 12 Dental Identifcation in Multiple Fatality Incidents 245 Bryan Chrz 13 Age Estimation from Oral and Dental Structures 263 edward F. Federal and State Court Cases of Interest in Forensic Odontology 411 Compiled By hasKell m. Barsley Index 423 Preface Since the publication of the frst edition of Forensic Dentistry in 1997 the discipline of forensic odontology has experienced considerable growth. Like all forensic specialties, forensic dentistry or forensic odontology has enjoyed (some may say sufered) a great increase in public interest during this period. Forensic dentists assist medical examiners, coroners, police, other law enforcement agencies, and judicial ofcials to understand the signifcance of dental evidence in a variety of criminal and civil case types. Prosecution, plaintif, and defense attorneys rely on forensic odontologists to analyze, report, and explain dental fndings that impact their cases. Te growth and evolution of forensic odontology has not taken place without signifcant growing pains. Te editors and contributors have chosen not to attempt to rationalize those problems but to report them, analyze the causes, and ofer alternate courses to minimize the probability of similar dif- fculties in the future. Te editors did not intend for this book to include comprehensive, step- by-step instructions on how to practice each phase of forensic odontology. Instead, the editors and contributors have endeavored to look objectively and philosophically at the development, current state, and future of forensic dentistry and other closely associated forensic disciplines. We are of the mind that if sound scientifc principles are applied from the beginning, and continued throughout, then the specifc steps taken will follow that same model and will have the best opportunity to meet success. Tey have produced thoughtful and sometimes provocative chapters that ofer substance, fact, and ideas suitable for experienced forensic investigators or those who are just embarking on forensic careers. Te editors want to ofer particular thanks to our families and especially to our wives, who not only gave us gracious support, but endured, mostly graciously, our extended physical, emotional, and mental absence. He practiced general dentistry from 1969 until 1992 and has practiced and taught forensic odontology exclusively since 1992. He is director, Center for Education and Research in Forensics; director, Fellowship in Forensic Odontology; and director, Southwest Symposium on Forensic Dentistry. He has authored book chapters and articles in refereed journals on forensic odontology topics. He is a forensic odontology consultant and chief forensic odontologist for the Bexar County (Texas) Medical Examiner’s Ofce. He serves on the board of editors for the American Journal of Forensic Medicine and Pathology and is an editorial consultant for Forensic Science International. He has served on the board of governors for the American Society of Forensic Odontology, currently serves on the board of directors of the Forensic Specialties Accreditation Board, and is the president (2009–2010) of the American Board of Forensic Odontology. He is an emeritus professor in the Department of Oral and Maxillo- facial Pathology at the University of Texas Dental Branch in Houston. He began his teaching career there afer completing graduate school in 1965, retiring in 1997. He taught oral and general pathology and forensic odon- tology and was an oral pathologist afliated with M. In 1968, he became the forensic odontologist for the Harris County Medical Examiner. He is pres- ently the chief consultant in forensic odontology for the medical examiner. He has taught forensic odontology for over forty years, and has written ref- ereed journal articles, book chapters, and edited books on this subject. He xi xii the editors taught in the forensic odontology course at the Armed Forces Institute of Pathology from 1968 until 1998. He was one of the founding fathers of the American Society of Forensic Odontology and has held every ofce in that organization in the earlier years of the society. He has held every ofce in that organization and has served on various study groups and committees. He is a registered emeritus diplomate of the American Board of Oral and Maxillofacial Pathol- ogy and an active diplomate of the American Board of Forensic Odontology. Frost Division of Oral and Maxillofacial Chief Medical Examiner Pathology Bexar County Medical Examiner’s Ofce College of Dentistry San Antonio, Texas University of Tennessee Memphis, Tennessee Harrell Gill-King Center for Human Identifcation Robert E. Golden New Orleans Forensic Center Deputy Coroner Orleans Parish Coroner Chief Forensic Odontologist New Orleans, Louisiana County of San Bernardino San Bernardino, California Paula C. Harris University of Texas Health Science Center at Professor San Antonio Department of Orthodontics and San Antonio, Texas Department of Pediatric Dentistry College of Dentistry Bryan Chrz University of Tennessee Consultant to the Ofce of the Chief Memphis, Tennessee Medical Examiner State of Oklahoma John D.

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Effect compartment or link models are limited If the partition coefficient order fluconazole 200 mg online fungus gnats traps homemade, Kp purchase 50mg fluconazole with visa zinsser anti fungal paint, equals Ce/C at equi- by their applicability to situations in which the librium (steady state) generic fluconazole 50 mg antifungal underarm cream, then we can rearrange the equilibrium between plasma and response is due above equation: to distributional phenomena order 150 mg fluconazole fast delivery fungus gnats cannabis. In reality, there is k V often a delay between occurrence of maximum 1e 1 Ve ¼ drug concentration in the effect compartment and Kpke0 maximum intensity of effect caused by slow devel- Substituting for V in the above equation opment of the effect rather than slow distribution to e (i. The plasma kinetics of (S)-warfarin were described by the fol- This is how the link-model relates the kinetics in lowing mono-exponential expression: plasma to the kinetics of drug in the effect compart- ment. The time to steady state is only governed by 120 the elimination rate constant and not the rate of infusion. It was also possible to estimate As stated before, the intensity of a pharmacologi- the half-life of the apparent first-order degradation. Rather, it may be the net allow for distributional effects embedded in the result of several processes only one of which is observed time delay of the onset of the effect influenced by the drug. The process that is influ- after warfarin administration, was published by enced by the drug must be identified and an Pitsui et al. Setting the baseline value of attempt be made to relate plasma drug concentra- clotting factor activity in the absence of warfarin tion to changes in that process. Warfarin provides a (P0) to a fixed mean of three predose measure- good example of this, as the anticoagulant (hypo- ments, the program can estimate that parameter. Precision increased of compounds emerging from medicinal chemistry when a finite lag time was included in the fitting. These detract from their value in chemical, structure– two cases, however, are especially relevant to the activity analyses). Neither does any of these relationship between animal work and phase I studies approaches uses results of invitro functional assays in which only the simplest effects, such as counter- which emerge from screening of the compounds in action of a painful stimulus or raising/lowering of a biochemistry laboratories. This is a postgraduate textbook, and we wish to convey how in vitro and in vivo data In the future, models will exist which will link of various kinds may be used to help extrapolate constants for in vitro binding to cloned human observed drug effects from simple experimental receptors (Kd), data from in vitro functional assays systems to the more complex clinical situation. The ultimate need is to obtain useful predictions A composite prediction matrix will be applied of response in healthy human subjects (phase I rapidly and accurately to the process of synthesis studies) from observed drug effects in animals or of new compounds for phase I testing. In the shorter term, what can we now do to What are the strengths and weaknesses of these expedite the drug selection process? The use of intrinsic clearance in vitro represents a flow chart illustrating one form of permits predictions between species for the parti- metabolism/pharmacokinetics input into the drug cular enzyme/route of metabolism concerned. Arrows (indicating the flow of humans have qualitatively different routes of work and communication) pointing to the right metabolism for any particular compound, then represent perceived progress, whereas arrows point- this will weaken the predictive value of the in ing tothe leftrepresent ‘disappointments’ (and other vitro observation. The works best for compounds with a high component numbered asterisks indicate continuations. The of nonenzymatic elimination, such as our model ‘flow of time’ is from left to right and from the top compound with approximately 90% excretion as panel to the bottom panel. This prediction weakens as var- tasks that are to be completed, and rectangles in a iations in rates of enzymatic reactions become column within a panel represent work done by more important. If preclinical work identified metabolite(s) to and may not necessarily be based on hard and fast measure in humans, are the pharmacokinetics criteria. Does the relationship between concentration compounds that have the same indication. For example, within the represents the tasks that can be expedited by online box including ‘in vitro intrinsic clearance’, there pharmacokinetic modeling. Among the pharmaco- may be in vitro predictors of oral availability and kinetic questions that will be asked online in the measures of potentially toxic metabolites. The ‘in phase I trial are the following: vivo pharmacokinetics’ in rats may include an increasing number of compartments whose con- 1. As the doses are escalated, do the kinetics of the centrations are measured by microdialysis and may drug appear to be linear or nonlinear over the include measures of a few selected metabolite dose range? However, it does show that the change in kinetics, for example a higher elim- chemists discover new chemical entities with ination rate that might be indicative of autoin- desirable properties. This is not a comprehensive flow diagram for all aspects of drug discovery – it is restricted to the components of the process discussed in this chapter. In this context, phase I serves as the As a chemical series develops, correlations such interface between preclinical research and clinical as that in Figure 8. Eventually, a development, and the validity of the predictions compound or compounds is/are chosen for phase I from animals to humans involved is of paramount studies. In this scheme, phase I is influenced by pharma- We believe that with enhanced integrated study cokinetic and pharmacodynamic modeling. The objective is expe- lism and pharmacokinetics (Welling and Tse, ditious choice of the best compound, with the ever- 1995). The time saved could be used to permit a present limitations on information available. Note larger number of compounds with better pro- that this scheme can involve feedback from phase I spects, from a single research program, to be to renewed chemical synthesis, as well as choice of compared in phase I studies. Typically, after adequate preclinical char- acterization of a candidate drug and 14-day and/or 3-month multiple-dose toxicology studies in two References mammalian species, a very low dose is chosen for the first human exposure to the drug. Doses may be single or short multiple- netics: the dynamics of drug absorption, distribution dose series. PharmacokineticandPha- a-adrenergic receptors and contraction of rat vas rmacodynamic Data Analysis: Concepts and Applica- deferens’. Interspecies scaling and comparisons Pharmacokinetic/Pharmacodynamic Analysis: in drug development and toxicokinetics. Financial pressures, even for the largest pharma- model ceutical companies, are generally much greater than in the past. The technical response is to max- In former times, it was assumed that developmental imize resources, avoiding any and all redundant drugs proceeded in stepwise fashion from phase I, clinical studies. Phase I was conducted in ‘normal volun- the regulatory authorities and from within the teers’ (although some medical students might pharmaceutical companies themselves. After approval, certain stu- earlier stages of drug development when these dies, to find new indications, address special questions are asked, have driven change in patient subpopulations, for marketing purposes or clinical study design. Increasingly sophisticated to otherwise broaden product labeling might or data are now developed at earlier stages of drug might not be conducted. Strategies such as the overlapping of devel- any generally agreed definitions except, perhaps, opment ‘phases’, as well as the use of early dose- that the studies are run by different teams. None of are (and always have been) sound medical or phar- today’s successful companies actually use such a macological reasons for doing so. It would be unreasonable to study the pharma- cokinetics of relatively toxic agents, at poten- 9. Typically, this information can be gained in Bias is a general consideration in clinical trial patients with diseases potentially responsive to design, regardless of the type of trial being con- these agents. Cytotoxic and antiviral drugs are two of the types of study design considered below. This enemy comes from many quarters doses at which tolerability must be confirmed are (Table 9. The clinical trialist must be sufficiently unknown until the exposure of patients can indi- humble to realize that he or she, himself or herself, cate the doses that may be effective. However, the ability to talk to and understand statisticians is There are some diseases which have neither ani- absolutely essential. Sine qua non: Involve a mal model nor relevant pharmacodynamic or sur- good statistician from the moment a clinical trial rogate end point in normal volunteers. This is one of your best defences against migraine, and normal volunteers cannot report an bias.

For nurses with specialist neurological training generic 150 mg fluconazole visa antifungal toe cream, these conditions can create very real challenges buy generic fluconazole 200 mg fungus edh deck, which—more than in many pathological conditions—are largely resolved by nursing rather than medical interventions discount 200mg fluconazole fungus bacteria. Useful contact The Guillain Barré helpline: 0800 374803 Further reading Useful medical articles on Guillain Barré syndrome include Desforges (1992) and Fulgham & Wijdicks (1997) literature reviews discount 150 mg fluconazole with amex fungus resistant materials, Hund et al. Finocchiaro and Herzfeld (1990) provide almost the only easily accessible nursing article on autonomic dysreflexia; Keely (1998) gives a useful critical care update. Some have been published in nursing and medical journals, but can be difficult to obtain. Clinical scenario Duncan Munro, 46 years old, presented with tachypneoa (over 40 breaths/min), tachycardia (110 beats/min), hypertension (170/110 mmHg), difficulty swallowing, general fatigue with numbness in both legs and feet. During the previous three weeks, he had been travelling abroad on business and recovering from an upper respiratory tract infection. Duncan’s respiratory and motor function deteriorated a tracheotomy was performed Neurological pathologies 375 and invasive positive pressure ventilation initiated. The liver has more functions, and a wider range of functions, than any other major organ, so that hepatic failure causes many problems. Liver function tests indicate the degree of liver failure; if severe, referral to specialist centres may be necessary. The term fulminant hepatic failure (liver disease together with encephalopathy occurring within 8 weeks of onset) is still used, but it is increasingly being replaced by ■ hyperacute (0–7 days) ■ acute (8–28 days) ■ subacute (29 days-12 weeks). Although scientifically questionable (drugs are chemicals), this apparently arbitrary division is clinically useful. Symptoms of acute failure are similar from all causes, but are included here in the section on paracetamol. Many other therapeutic drugs (such as chlorpromazine) can also provoke failure (Hawker 1997a). Hepatic failure 377 Hepatic failure may be caused by hepatitis and many other viruses (e. Hepatocyte recovery is good following acute hepatic failure, and so treatment is largely a matter of system support to minimise complications (especially cerebral oedema and cardiac failure) and allow hepatocyte recovery. Progression to chronic failure usually causes ■ hyperdynamic circulation ■ portal hypertension ■ oesophageal varices and bleeding. Survivors of these complications usually progress to end-stage failure, necessitating transplantation (see Chapter 44). Most of the complications identified here occur with acute failure, but some complications of chronic failure are also specifically identified. Plasma paracetamol levels exceeding 250 mg/litre after 4 hours or 50 mg/litre at 12 hours usually result in hepatic damage (Weekes 1997), although severe symptoms may be delayed for 2–3 days, appearing only after significant, possibly fatal, damage. Human transmission is only through faeces (not blood or other body fluids), infection being endemic where sanitation is poor (Pratt 1995). Transmission can be ■ parenteral (most body fluids) ■ sexual ■ (possibly) through insect bites (Pratt 1995). Chronic carriers rarely develop infection (Raeside 1996), but can spread infection (Pratt 1995). Hepatitis C usually recurs following transplantation, but most patients remain asymptomatic. Hepatitis D complicates hepatitis B infection, making fulminant hepatic failure more likely. In Europe and North America, hepatitis D is primarily transmitted through drug injection; elsewhere infection is usually sexual (Pratt 1995). Hepatic failure 379 Complications Liver dysfunction affects most other major systems of the body. The description below is reductionist, and specific management of other systems is covered in other chapters. Cerebral oedema provokes intracranial hypertension, impairing cerebral perfusion pressure (see Chapter 22). Prolonged effects from exogenous sedation may delay recovery and make assessment difficult; debate continues on whether to avoid sedating patients with hepatic failure. Whichever medical practice is followed, nurses should actively assess the level of sedation and effects of drugs. Normal sleeping patterns may be reversed, with patients remaining awake overnight. Treatment should optimise cerebral perfusion pressure by reducing intracranial pressure while maintaining mean arterial pressure (see Chapter 22). Persistent intracranial hypertension (above 25 mmHg) may be reversed with mannitol. Chronic failure compounds dyscrasias from ■ splenatomegaly (from portal hypertension), which reduces platelet counts ■ depressed bone marrow function (from alcoholism or paracetamol) which reduces erythropoiesis. Gastrointestinal and respiratory (although not cerebral) bleeds frequently occur (Hawker 1997a). Replacement factors, such as vitamin K (Cowley & Webster 1993) or blood components, may be prescribed. Intensive care nursing 380 The liver contributes significantly to immunity through production of complements (see Chapter 23) and Kupffer cells—specialised reticuloendothelial cells in the liver which destroy any bacteria translocating from the gut. Asepsis, high standards of infection control and continuing vigilance can minimise risks to patients; early detection of infection enables early treatment. Blood from the liver soon reaches pulmonary vessels so that surviving gut bacteria readily cause pulmonary infection; increased capillary permeability enables pulmonary oedema formation, and possible shunting. As suction raises intracranial pressure, patients should be preoxygenated and duration and number of passes should be minimised (see Chapter 22). Suction may also cause trauma, so that catheters withdrawn should be observed for blood (type, amount) as well as sputum (type, colour, amount). Hepatopulmonary syndrome occurs in up to 30 per cent of patients with endstage failure (Isaac & Manji 1997). Pathology is unclear; there is no specific treatment and resolution can be spontaneous, but mortality remains high. Hepatopulmonary syndrome is an indication for liver transplantation (Isaac & Manji 1997. Cardiovascular compromise is caused by ■ hypovolaemia ■ vasodilation ■ increased capillary permeability ■ reduced cardiac return. As prolonged hypotension predisposes to multiorgan dysfunction, nurses should closely assess and monitor cardiovascular function. Inotropes will probably be needed, although may have little effect if sympathetic pathways are damaged. Stress responses (see Chapter 3) increase blood and intracranial pressure, and so patients should be nursed in quiet environments with minimal sensory stimulation. There is no detectable histological change to renal tissue, and kidneys resume normal function following hepatic transplantation (Hinds & Watson 1996); without transplantation, mortality exceeds 90 per cent (Hinds & Watson 1996). Unlike acute tubular necrosis, relatively normal sodium reabsorption and urine concentration is maintained during hepatorenal syndrome. The liver has more than 500 metabolic functions, and so hepatic failure causes complex disorders. Electrolyte disorders from hepatic hypofunction are often compounded by renal and capillary epithelial changes. Reduced free water clearance can dilute electrolyte concentrations, causing hyponatraemia and hypokalaemia (Sussman 1996).

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