Handbook of Forensic Medicine E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Wissenschaft und neue Technologien
- Sprache: Englisch
Forensic Medicine encompasses all areas in which medicine and law interact. This book covers diverse aspects of forensic medicine including forensic pathology, traumatology and violent death, sudden and unexpected death, clinical forensic medicine, toxicology, traffic medicine, identification, haemogenetics and medical law. A knowledge of all these subdisciplines is necessary in order to solve routine as well as more unusual cases.
Taking a comprehensive approach the book m.oves beyond a focus on forensic pathology to include clinical forensic medicine and forensic toxicology. All aspects of forensic medicine are covered to meet the specialist needs of daily casework. Aspects of routine analysis and quality control are addressed in each chapter. The book provides coverage of the latest developments in forensic molecular biology, forensic toxicology, molecular pathology and immunohistochemistry.
A must-have reference for every specialist in the field this book is set to become the bench-mark for the international forensic medical community.
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Seitenzahl: 4305
Veröffentlichungsjahr: 2014
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Table of Contents
Title page
Copyright page
Contributors
Preface
Foreword
PART I: Duties of Forensic Medicine in Modern Societies
1: History of Forensic Medicine
1.1 Definitions
1.2 Civilisations of the Near East and China
1.3 Justinian Enactments
1.4 Further Developments and Italian Town Charters
1.5 Forensic Medicine as a Book Science
1.6 Forensic Medicine as an Experimental Science
1.7 Current Problems
References and Further Reading
2: Duties of Forensic Medicine
References and Further Reading
3: Forensic Medicine and Human Rights
3.1 Human rights issues
3.2 Torture
Useful Websites
4: International Guidelines and Accreditation in Forensic Medicine
4.1 Introduction
4.2 Recommendations for Forensic DNA laboratories Based On ISO/IEC 17025
4.3 Recommendations for Forensic Toxicological Laboratories Based On ISO/IEC 17025
4.4 Recommendations for Forensic Pathology Based On ISO/IEC 17025
4.5 Recommendations for Clinical Forensic Medicine Based On ISO/IEC 17020
Useful websites
References and Further Reading
PART II: Medical Aspects of Death
5: Nature and Definition of Death
5.1 Death and Dying
5.2 Determination of Death
References and Further Reading
6: Certification of Death: External Postmortem Examination
6.1 Introduction
6.2 Cause of Death
6.3 Causes of Death as Shown by Cause of Death Statistics
6.4 Consistency between Cause of Death Diagnosis on the Death Certificate and Following Autopsy
6.5 Manner of Death
6.6 Special Constellations of Circumstances in External Postmortem Examination
6.7 Checklist for the External Postmortem Examination (according to Madea 2006)
6.8 Identification of the Corpse
6.9 Examination of the Corpse
6.10 Completing the Death Certificate
Useful Website
References and Further Reading
7: Postmortem Changes and Time Since Death
7.1 Early Postmortem Changes
7.2 Later Postmortem Changes: Decomposition
7.3 Timing of Death
7.4 Basic Forensic Entomology
7.5 Postmortem Injuries
7.6 The Physician and the Crime Scene
Note
References and Further Reading
8: Cremation
8.1 Short History of Cremation
8.2 Cremation in the Modern Day
8.3 Process of Cremation and Modification of the Corpse during Cremation
8.4 Remnants of Cremation
8.5 Conclusions
References and further reading
9: Autopsy
9.1 Introduction
9.2 Medicolegal Autopsy
9.3 Clinical Autopsy
9.4 Autopsy Report
9.5 Forensic Imaging
Acknowledgements
Useful Websites
References and Further Reading
10: The Doctor, the Dead and Their Relatives
10.1 Pronouncing Life Extinct and Informing the Next of kin about a Death
10.2 Role of the Deceased
10.3 Respect for Taboos and Propriety
10.4 Manner of Death and Police Investigations
10.5 Dealing with the Relatives
References and Further Reading
11: Transplantation
11.1 Regulations and Procedures in Germany
11.2 Legal Prerequisites and Procedures in the UK
11.3 Criteria for the Diagnosis of Brain Death in the UK
11.4 Special Forensic Medical Aspects of Organ Donation and Tissue Retrieval
Useful Websites
References and Further Reading
12: Anthropology and Osteology
12.1 Introduction
12.2 Preliminary Steps
12.3 Diagnosis of Species
12.4 Biological Profile: The Main Role of Anthropology
12.5 Facial Reconstruction
12.6 Geographical Origin
Useful Website
References and Further Reading
13: Mass Disaster Victim Identification
13.1 Introduction
13.2 International Cooperation
13.3 DVI Team Structure
13.4 Standardisation
13.5 Forensic Odontology Standards
13.6 Forensic Molecular Biology Standards
13.7 Radiology Standards
13.8 Chemical Biological Radioactive Nuclear Explosive Weapons
13.9 Documentation and Quality Management
Useful Websites
References and Further Reading
PART III: Traumatology and Violent Death
14: Legal Aspects of Traumatology and Violent Death
14.1 Definitions
14.2 Basic Legal Principles
14.3 Conclusions
15: Traumatology and Criminology
15.1 Introduction
15.2 Homicide
15.3 Non-Homicidal Events
15.4 Suicide
15.5 Torture
15.6 Homicide, Suicide or Accident?
16: Introduction to Some Biomechanical Principles
16.1 Introduction
16.2 Separation of Coherence Through the Impact of Tensile Stress
16.3 Separation of Coherence Through the Impact of Shear Stress
17: Sequelae of Traumatic Injuries and Causes of Death
17.1 Introduction
17.2 Sepsis and Multiple Organ Failure
References and Further Reading
18: Vital Reactions and Wound Age Estimation
18.1 Vital Reactions
18.2 Wound Age Estimation: General Introduction and Methods
18.3 Wound Age Estimation: Molecular Biology
References and Further Reading
19: Mechanical Trauma and Classification of Wounds
19.1 Classification of Violence
19.2 Blunt Force Injury
19.3 Forensic Neuropathology
19.4 Sharp Force Injury
Acknowledgements
References and Further Reading
20: Forensic Ballistics: Injuries from Gunshots, Explosives and Arrows
20.1 Introduction
20.2 Firearms
20.3 Arrow Wounds
20.4 Explosive Injuries
References and Further Reading
21: Injuries due to Asphyxiation and Drowning
21.1 Asphyxiation
21.2 Drowning
21.3 Barotrauma and Diving-Related Accidents
21.4 Immersion Time
Useful Website
References and Further Reading
22: Injuries due to Heat
22.1 Introduction
22.2 Burns from Heat
22.3 Causes of Death from Heat
22.4 Scalding
22.5 Generalised Heat Damage and Hyperthermia
22.6 Diagnosis
References and Further Reading
23: Injuries due to Cold
23.1 Introduction
23.2 Pathophysiology
23.3 Clinical Phases of Hypothermia
23.4 Epidemiology
23.5 Morphological and Biochemical Changes
23.6 Criminal Aspects
References and Further Reading
24: Electrocution and Lightning
24.1 Electrocution
24.2 Lightning
Useful Websites
References and Further Reading
25: Starvation and Neglect
25.1 Introduction
25.2 Clinical and Autopsy Findings in Starvation
25.3 Classification Systems
25.4 Death from Starvation
25.5 Physical Neglect
References and Further Reading
26: Infanticide
26.1 Introduction
26.2 Stillbirth
26.3 Neonaticide
26.4 Investigation of Mothers and Neonates
References and Further Reading
27: Death during Pregnancy
27.1 Analysis of Maternal Mortality
27.2 Pregnancy as a Physiological Process with Specific Risks
27.3 Maternal Death Directly Due to Gestation
27.4 Maternal Death Indirectly Due to Gestation
27.5 Iatrogenic Maternal Death
27.6 Maternal Death Not Due to Gestation
Useful Websites
References and Further Reading
28: Auto-Erotic Death
28.1 General Aspects
28.2 Categorisation of Death Cases
28.3 Possible Mechanisms of Death
28.4 Typical Injuries to Male Genitalia and Special Cases
References and Further Reading
29: Death in Abnormal Positions: Physical Restraint
29.1 Custody and Restraint Death
29.2 Extrinsic Factors
29.3 Intrinsic Factors
29.4 Controversies: Excited Delirium
29.5 Investigation of Death in Custody: Restraint and Body Position
29.6 Certification of Death
References and Further Reading
30: Sexual Homicide
30.1 Introduction
30.2 Profiling Offenders in a Sex-Related Homicide
30.3 Crime Assessment
30.4 Conclusions
References and Further Reading
31: Medical Malpractice
31.1 Introduction
31.2 Definitions
31.3 Epidemiology
31.4 Value of Autopsies
31.5 New Approaches
31.6 Conclusions
References and Further Reading
32: Special Issues Regarding Expert Evidence in Violent Death
32.1 Priority and Order of Injuries
32.2 Physical Activity after Injuries and Survival Time
32.3 Postmortem Mutilation
32.4 Alcohol-Related Deaths
32.5 Death Due to Drug Addiction
32.6 Mafia-Related Deaths
References and Further Reading
PART IV: Sudden and Unexpected Death from Natural Causes
33: Natural Causes of Sudden Death
33.1 Introduction
33.2 Cardiac Causes of Sudden Death
33.3 Non-Cardiac Causes of Sudden Death
References and Further Reading
34: Postmortem Biochemistry as an Aid in Determining the Cause of Death
34.1 Introduction
34.2 Glucose Metabolism and Diabetes Mellitus
34.3 Alterations of Liver Function
34.4 Disturbances of Kidney Function
34.5 Water and Electrolyte Imbalances
34.6 High Excitation and Hypothermia
34.7 Chronic Alcoholism
34.8 Anaphylactic Shock
34.9 Genetic Alterations
34.10 Conclusions
References and Further Reading
35: Sudden and Unexpected Deaths in Infants and Sudden Infant Death Syndrome
35.1 Introduction
35.2 Sudden Infant Death Syndrome
35.3 Other Main Causes of Death in SUDI Cases and During Childhood
35.4 Practical Investigation of SUDI/SIDS
35.5 Conclusions
References and Further Reading
PART V: Clinical Forensic Medicine
36: Sexual Abuse
36.1 Introduction
36.2 Examination of the Victim
36.3 Sexually Transmitted Infections
36.4 Toxicological Analysis
36.5 Legal Outcome
36.6 Juvenile Pornography
Appendix 36.1 Approach to Interpretation of Medical Findings in Suspected Sexual Abuse
Appendix 36.2 Reminder Checklist
References and Further Reading
37: Non-Sexual Abuse in Children
37.1 Non-Accidental Head Injury in Children
37.2 Child Abuse
References and Further Reading
38: Intimate Partner and Domestic Violence
38.1 Introduction
38.2 Causes and Reasons for Domestic Violence
38.3 Effects and Consequences of Domestic Abuse
38.4 The Cycle of Violence
38.5 Diagnostic Procedures
38.6 Human Immunodeficiency Virus and Domestic Abuse
38.7 Challenges Facing Older Women
References and Further Reading
39: School Violence
39.1 Introduction
39.2 Statistical Data from Various Countries
39.3 Motives and Reasons for School Violence and Its Identification
39.4 Prevention and Interventional Procedures
References and Further Reading
40: Violence Against Homosexuals
40.1 Introduction
40.2 Characteristics of Gay Violence
40.3 Violence in Straight Versus Homosexual Relationships
40.4 Problems with Statistical Data and Underlying Causes
References and further reading
41: Violence Against the Elderly
41.1 Introduction
41.2 Definition and Scope of Elder Mistreatment
41.3 Types of Abuse of the Elderly
41.4 Mimics of Elder Abuse
41.5 Clinical Evaluation in Living Patients
41.6 Medicolegal Investigations
41.7 Conclusions
Useful Website
References and Further Reading
42: Self-Harm
42.1 Definitions, Phenomenology and Underlying Causes
42.2 Historical Aspects, Epidemiology and Statistical Data
42.3 Classification and Phenomenology of Self-Harm Groups
42.4 Diagnostic Procedures
Useful Website
References and Further Reading
43: Age Estimation in Living Individuals
43.1 Introduction
43.2 Age estimation in adolescents and young adults
43.3 Influence of Ethnicity on Development
43.4 Expert Reports
43.5 Age Estimation in Child Pornographic Images
43.6 Age Estimation in Old Age Proceedings
43.7 Quality Assurance
Useful Website
References and Further Reading
PART VI: Forensic Psychiatry
44: Forensic Psychiatry
44.1 Definitions
44.2 Inquisitorial Versus Adversarial Legal Systems
44.3 Forensic Psychiatry Examinations
44.4 Civil law, Competencies and General Legal Competency
44.5 Competencies in Criminal Law
44.6 Criminal Responsibility
44.7 Forensic Security Hospitals
44.8 Formal Education in the Subspeciality of Forensic Psychiatry
44.9 Conclusions
Legislation (Codes and Statutes)
Landmark Court Cases (Rulings and Opinions)
References and further reading
PART VII: Toxicology
45: Legal Aspects of Toxicology
45.1 Introduction
45.2 Administrative Issues
45.3 Abused and Controlled Substances
45.4 Postmortem Toxicology
45.5 Clinical Forensic Toxicology
45.6 Doping
45.7 Sabotage, Terrorism and Chemical Warfare
Useful Websites
References and Further Reading
46: Epidemiology and Adverse Drug Reactions
46.1 Introduction
46.2 Adverse Drug Reactions and Side Effects
46.3 Inherent Toxicity of a Substance
46.4 Epidemiology
46.5 Evidence Basis for Toxicity
46.6 Conclusions
Useful Website
References and Further Reading
47: Suspicion of Poisoning
47.1 Diagnosis of Acute Poisoning
47.2 Specimen Collection for Forensic Toxicology
47.3 Clinical Signs and Syndromes in Intoxication
Useful Websites
Note
References and Further Reading
48: Toxicological Analysis: Drug Screening and Confirmation
48.1 Introduction
48.2 Screening and Confirmation Tests
48.3 Isolation Step
48.4 Instrumentation Used in Forensic Toxicology
48.5 Analytical Methods
48.6 Method Performance
Useful Websites
References and Further Reading
49: Issues Affecting Interpretation: Stability and Artefacts
49.1 Introduction
49.2 Definition of Stability and Common Causes of Instability and Artificial Formation
49.3 Stability of Drugs and Potential Artefacts
49.4 Sampling Artefacts and Measures to Increase Drug Stability
49.5 Influence of Storage
49.6 Instability of Drugs and Artificial Formation During Processing and Analysis
49.7 Procedures for Evaluating Stability and Artefacts
49.8 Conclusions
References and Further Reading
50: Toxicokinetics and Toxicogenetics
50.1 Introduction and the LADME Principle
50.2 Basic Kinetic Parameters
50.3 Toxicokinetics and Toxicogenetics in Forensic and Clinical Toxicology
50.4 Release
50.5 Absorption
50.6 Distribution
50.7 Metabolism
50.8 Excretion
50.9 Conclusions
References and Further Reading
51: Toxicology of Specific Substances
51.1 Alcohols
51.2 Illegal Drugs
51.3 Sedatives and Hypnotics
51.4 Narcotics and Other Analgesics
51.5 Toxic Elements
51.6 Solvents and Gaseous Poisons
51.7 Natural Poisons
51.8 Pesticides and Insecticides
51.9 Doping
Useful Websites
References and Further Reading
PART VIII: Traffic Medicine
52: Driving Aptitude and Fitness to Drive
52.1 Introduction
52.2 Definitions and Operationalisation
52.3 Factors Influencing Driving Aptitude and Fitness to Drive
52.4 Assessment of Driving Aptitude and Fitness to Drive
References and Further Reading
53: Effects of Cardiovascular Disease on Fitness to Drive
53.1 Introduction
53.2 Derivation of the Risk of Harm Formula
53.3 Coronary Heart Disease
53.4 Arrhythmias
53.5 Syncope
53.6 Heart failure
References and Further Reading
54: Effects of Vision and Visual Fields on Fitness to Drive
54.1 Introduction
54.2 Problems with Vision
54.3 Visual Field Disorders
54.4 Condition after an Eye Operation
54.5 Problems of Vision in Older Motorists
54.6 Effects of Visual Deficiencies
References and Further Reading
55: Effects of Epilepsy on Fitness to Drive
55.1 General Rules
55.2 Background
55.3 Legal Aspects
55.4 Epilepsy and General Road Safety
55.5 Outlook
References and Further Reading
56: Effects of Diabetes on Fitness to Drive
56.1 Classification of Diabetes
56.2 Stages of Diabetes
56.3 Driving and Treatment of Diabetes
56.4 Driving Performance and Diabetes
56.5 Therapeutic Aspects for Driving Safely with Diabetes
References and Further Reading
57: Epidemiology and Causal Factors in Fitness to Drive
57.1 Introduction
57.2 Epidemiological Methods
57.3 Examples of Epidemiological Studies
References and Further Reading
58: Effects of Alcohol on Fitness to Drive
58.1 Introduction
58.2 Medicolegal Alcohol Determination
58.3 Characteristics of Offenders
58.4 Amounts of Alcohol Consumed
58.5 Alcohol Consumption and Crash Risk
58.6 Alcohol Tolerance
58.7 Conclusions
References and Further Reading
59: Effects of Illegal Drugs on Fitness to Drive
59.1 Introduction
59.2 Problems Regarding Epidemiological Data
59.3 Effects of Drugs on Driving
59.4 Forensic Toxicological Analyses
References and Further Reading
60: Effects of Medicinal Drugs on Fitness to Drive
60.1 Introduction
60.2 Medicinal drugs that impair driving
60.3 Conclusions
References and further reading
61: Toxicological Markers of Chronic Alcohol Abuse
61.1 Introduction
61.2 Overview and Characteristics of Alcohol Biomarkers
61.3 Biomarkers of Alcohol Consumption
61.4 Detection of Chronic Excessive Alcohol Consumption
61.5 Control of Abstinence
References and Further Reading
62: Traffic Accidents
62.1 Road Traffic Accidents
62.2 Sudden Death While Driving
62.3 Suicide While Driving
62.4 Railway Accidents
62.5 Aircraft Accidents
62.6 Mass Disasters
Useful Websites
References and Further Reading
PART IX: Identification
63: Forensic DNA Analysis
63.1 Stain Analysis
63.2 Paternity Testing
Useful Websites
References and Further Reading
64: Forensic Anthropology
64.1 Introduction
64.2 Identification of Human Remains
64.3 Identification of the Living
References and Further Reading
65: Forensic Odontology
65.1 Introduction
65.2 Dental Charting
65.3 Age Estimation
65.4 Identification of an Unknown Person
65.5 Bite Marks
References and Further Reading
PART X: The Doctor and the Law
66: The Doctor and the Law
66.1 Legal Relevance of Medical Treatment
66.2 Legal Aspects of Personalised Medicine
66.3 Assisted Suicide and Organised Medically Assisted Suicide
66.4 Research on Corpses
66.5 Legal and Ethical Aspects Concerning the Handling of Corpses and the Display of Human Remains
Acknowledgements
Notes
References and Further Reading
PART XI: Insurance Medicine
67: Personal Injury Assessment
67.1 Introduction
67.2 Aim of Personal Injury Assessment and Reparation
67.3 General Aspects for Forensic Medical Assessment
67.4 Specifics of Forensic Medical Reports for Personal Injury Assessment
67.5 Conclusions
References and Further Reading
Further Reading
Index
End User License Agreement
List of Tables
Table 1.1 Timetable of the history of forensic medicine.
Table 3.1 Torture methods reported by 235 torture victims from 35 different countries. Percentages exceed 100, as almost all victims had been tortured in many ways.
Table 4.1 Postgraduate professional education modules for the German ‘Forensic toxicologist GTFCh’ qualification.
Table 4.2 Recommendations for sampling prior to, or during, all autopsies or autopsies where the cause of death remains uncertain or special problems have to be addressed (GTFCh 2004).
Table 6.1 Function and importance of the external postmortem examination. Reproduced with permission from Madea (2006), © Springer.
Table 6.2 Terminology of death certification. Reproduced with permission from Myers and Farquhar (1998), © Canadian Medical Association.
Table 6.3 Final indirect causes of death. After Fyerter in Madea (2006), © Springer.
Table 6.4 Causes of death: examples and important aspects, according to the German Federal Statistical Office recommendations.
Table 6.5 Definition of major and minor errors in death certificates. Reproduced with permission from Myers and Farquhar (1998), © Canadian Medical Association.
Table 6.6 Case illustration showing types of mistake in stating the cause of death. Case scenario adapted with permission from Myers and Farquhar (1998), © Canadian Medical Association.
Table 6.7 Findings at the external postmortem examination in cases of intoxication. After Madea (2006), © Springer.
Table 7.1 Upper and lower confidence limits for the six degrees of electrical excitability in hours in different random samples: forensic pathology, clinical pathology and emphysema and haematoma of the eyelid.
Table 7.2 Postmortem excitability of the iris after the injection of different drugs.
Table 7.3 Lividity: causes, consequences and phenomena checked on the body.
Table 7.4 Postmortem lividity discoloration. After Spitz and Fischer (1993).
Table 7.5 Time course of different criteria of lividity according to calculations by Mallach (1964) based on textbook reports.
Table 7.6 Overview of the biochemical, mechanical, morphological and physiological bases of rigor mortis.
Table 7.7 Time course of different criteria of rigor mortis according to calculations by Mallach (1964) based on textbook reports.
Table 7.8(a) Empirical corrective factors (c.f.) for body weights. The listed values of c.f. apply to bodies of average weight (reference: 70 kg); in an extended position on a thermally indifferent supporting base. ‘Thermally indifferent’ supporting bases are, for example usual floors of rooms, dry soil, lawn or asphalt. In comparison, bases which appear more thermically insulating than heat conducting should additionally be taken into account.
Table 7.8(b) The influence of the kind of supporting base on the corrective factor (c.f.) can be summarised as follows.
Table 7.9 Chart of the dependence of corrective factors on body weight.
Table 7.10 Morphological changes in the putrefaction phase, showing above-ground exposure at 20–24°C (68–75°F) without insect infestation. This is only a rough indication for the sequence of putrefaction effects in cadavers exposed above ground at a relatively narrow range of temperature. Numerous variations are possible, depending, for example, on the body's build, the underlying surface, coverings and terminal illness (Berg 2004). Reproduced with permission from Berg et al. (1981), C.J. Bucher München und Luzern.
Table 7.11 Progression of the putrefaction of bodies in air, at a temperature of about 20°C. Reproduced with permission from Naeve in Madea (2006), © Springer.
Table 7.12 Table for estimation of the time since death based on supravital reactions and postmortem changes.
Table 7.13 Precision of time of death estimation using vitreous potassium in different random samples. Urea was used as internal standard; statistical parameters are shown of the entire sample and subgroups. The data in brackets are from Madea et al. (1989).
Table 7.14 The German forensic pathologist Reh (1969) developed this chart showing minimum time intervalsa of immersion (days).
Table 12.1 Correlation between diaphyseal length of different bones and age.
Table 12.2 Equations for stature estimation calculated from specific long bone lengths.
Table 13.1 Comparison of different dental schemes, with the number representing different codes specifying individual teeth.
Table 14.1 An example of how in Hong Kong the severity of injuries inflicted is directly linked to criminal liability and also the punishment imposed for the crime.
Table 15.1 The top five countries with the highest homicide rates from each of five continents in 2004. Rates are per 100 000 population. Data © United Nations Office on Drugs and Crime International Homicide Statistics.
Table 15.2 The five countries with the lowest homicide rates from each of four continents in 2004. Rates are per 100 000 population. Data © United Nations Office on Drugs and Crime International Homicide Statistics.
Table 18.1 Vital reactions – haemorrhages. The degree of haemorrhage depends on the size of the injured vessel, the blood pressure and the resistance to the blood that is streaming.
Table 18.2 Vital reactions – embolisms.
Table 18.3 Grading of fat embolism (FE). After Falzi et al. (1964).
Table 18.4 Vital reactions – aspiration/inhalation.
Table 18.5 Examples of wound age estimation by immunohistochemical methods in human skin lesions.
Table 18.6 Methodology for studying vitality and wound age estimation.
Table 18.7 Adhesion molecules.
Table 18.8 Cytokines, growth factors and stress protein.
Table 18.9 Extracellular matrix.
Table 19.1 Different types of external violence, wounds and trauma.
Table 19.2 Routine staining methods and immunohistochemistry methods for the detection of different cells and structures in forensic neuropathology.
Table 19.3 Time course of microscopic findings in cases of of contusional haemorrhages.
Table 19.4 Contusion index of haemorrhages of the human brain (see Adams et al. 1985).
Table 19.5 Time course of microscopic findings in cases of contusional haemorrhages.
Table 19.6 Different forensic types of hypoxia, ischaemia and asphyxia.
Table 19.7 Functional impairment of the brain in dependence of the duration of the disruption of oxygen supply. Reproduced with permission from Grote (1980), © Springer.
Table 19.8 Suicidal and homicidal case findings of sharp force injury.
Table 20.1 The mass and muzzle velocity of a selection of conventional pistol and revolver bullets. Approximate values from a broad range of different manufacturers are given. Energy values are deliberately not stated.
Table 20.2 The mass and muzzle velocity of a selection of rifle bullets for military and hunting purposes or both. Again, these are approximate values depending on the actual load of different manufacturers. Energy values are not stated because they are secondary to mass and velocity.
Table 21.1 General stages of asphyxiation. Modified from Ponsold and Berg (1967).
Table 21.2 Evaluations of the video documentation of 14 cases of hanging. From Sauvageau et al. (2011).
Table 21.3 Percentage of eye-witnessed fatalities among 2125 water-related deaths in south Finland (1987–2012).
Table 21.4 Postmortem submersion time and percentage of main postmortem macromorphological findings of drowning in south Finland (1987–2012).
Table 21.5 Combined weights of lungs and pleural exudates in witnessed drowning1 and control groups.
Table 21.6 Percentage of suicide notes, by sex and age, in 492 suicides by drowning in south Finland (1987–2012).
Table 21.7 Major diving activities: selected parameters.
Table 21.8 Lung volume, absolute pressure, and partial pressure of gases in function of depth (Boyle's and Dalton's law).
Table 21.9 Reh's table to estimate the minimum time interval of immersiona (days).
Table 22.1 Classification of burn sources.
Table 22.2 (a) Degree of burn and the main symptoms.
Table 22.2 (b) Burn wound classification.
Table 22.3 Mortality probability for various combinations of ages and burnt body surface (1 = 100%). After Herndon (1997) and Allgöwer et al. (1998).
Table 22.4 Effects of heat on the body and related external and internal findings. Reproduced with permission from Bohnert (2004), © Springer.
Table 22.5 Fire gases and their effects. Reproduced with permission from Daunderer (1982), © Deutsches Ärzteblatt, Ärzte-Verlag GmbH.
Table 22.6 Effects of fire on the skull. Reproduced with permission from Bohnert et al. (1998), © Elsevier.
Table 22.7 Effects of fire on the trunk and extremities. Reproduced with permission from Bohnert et al. (1998), © Elsevier.
Table 22.8 Crow–Glassman scale of burn-related destruction of the corpse. After Bohnert (2004).
Table 22.9 Differential diagnosis of accidental and non-accidental scaldings. After Madea and Schmidt (2007).
Table 22.10 Causes and symptoms of systemic heat injuries.
Table 22.11 Glossary of terms in heat-related illness. From Bouchama and Knochel (2002).
Table 22.12 Predisposing factors in classic heat stroke.
Table 22.13 Types of heat stroke.
Table 23.1 Clinical phases of hypothermia; in individual cases the progression of clinical symptoms may vary.
Table 23.2 Signs and symptoms with grades of hypothermia. Reproduced with permission from Nixdorf-Miller et al. (2006), © College of American Pathologists.
Table 23.3 Peripheral cold injuries: freezing and non-freezing injuries. Reproduced with permission from Nixdorf-Miller et al. (2006), © College of American Pathologists.
Table 23.4 Morphological changes in hypothermia, underlying pathophysiology and diagnostic significance.
Table 23.5 Pancreatic changes in hypothermia according to different authors. Reproduced with permission from Madea et al. (2008), © Springer.
Table 25.1 Daily requirements of calories in humans. From Bürger et al. (1969).
Table 25.2 Energy requirements in healthy children (male and female).
Table 25.3 Classification of malnutrition in adults by body–mass index (WHO 1999).
Table 25.4 Loss of total body weight (%) and loss of weight of internal organs (%) as a result of inanition in humans. Reproduced with permission from Madea and Banaschak (2004), © Springer; see this for study details.
Table 25.5 Loss of body weight (%) and loss of weight of internal organs (%) in relation to normal weight values for differrent age groups. Reproduced with permission from Madea and Lachenmeier (2005), © Elsevier.
Table 25.6 Classification of protein–energy malnutrition (PEM).
Table 25.7 Simplified classification of protein-calorie malnutrition.
Table 25.8 Grading of protein–energy malnutrition.
Table 25.9 Development of height and weight of the twins shown in Fig. 25.4 from birth to death; cause of death: starvation.
Table 25.10 Vitreous humour values.
Table 26.1 Incidence of neonaticide and infanticide in various countries.
Table 26.2 Investigation of the corpse of a newborn. Reproduced with permission from Bajanowski and Verhoff (2008), © Springer.
Table 26.3 Markers indicating good development and maturity of a newborn infant.
Table 26.4 Maceration of the fetus. Reproduced with permission from Kratter (1921).
Table 26.5 List of priorities differentiated for various types of cases. Reproduced with permission from Bajanowski and Verhoff (2008), © Springer.
Table 27.1 Level of the fundus of the uterus during the course of pregnancy and postpartum. Reproduced with permission from Stoeckel and Wagenbichler (1998).
Table 30.1 Four categories of offenders known to commit multiple murders over time. After Keppel and Birnes (2003).
Table 31.1 Adverse events in hospitalised patients – an international comparison.
Table 31.2 Medical Error Reporting System (MERS) of the German Medical Council. Nationwide statistics of the arbitration committees.
Table 31.3 Patients’ complaints, 2009 and 2010 (Medical Error Reporting System).
Table 31.4 The medical disciplines concerned, 2010 (Medical Error Reporting System).
Table 31.5 The most frequent mistakes, 2010 (Medical Error Reporting System).
Table 31.6 The most frequent single diagnoses in which medical malpractice was confirmed in 2010.
Table 31.7 Decisions of the arbitration committees on medical malpractice (in 2010) and severity of damage caused by the medical malpractice. Source: Medical Error Reporting System.
Table 31.8 Medical disciplines concerned in medical malpractice claims.
Table 31.9 Cause of medical malpractice accusation.
Table 31.10 Classification of medical malpractice accusation.
Table 31.11 Causes of preliminary proceedings according to analysed documents.
Table 31.12 Occupational group and number of confirmed medical malpractice cases and confirmed medical malpractice with confirmed causality for death.
Table 31.13 Distribution of malpractice charges by duration and site of treatment.
Table 31.14 Results of medical malpractice proceedings.
Table 31.15 Adverse events in blood transfusion: classification. Reproduced with permission from Leo and Pedal (2010), © Springer.
Table 31.16 Synopsis of acute transfusion reactions. Reproduced with permission from Leo and Pedal (2010), © Springer.
Table 31.17 Medical malpractice and drug therapy – types of mistakes.
Table 32.1 Causes of death; the distribution in a Danish study of alcoholics. Reproduced with permission from Thomsen (2007).
Table 32.2 Metabolic effects of alcohol.
Table 32.3 Drugs and mechanism of death.
Table 32.4 (a) Central nervous system depressants.
Table 32.4 (b) Central nervous system stimulants.
Table 32.4 (c) Other common drugs.
Table 33.1 Most frequent causes of adult sudden death. After de la Grandmaison (2006).
Table 33.2 Classification of primary cardiomyopathies. Reproduced with permission from Fineschi et al. (2010).
Table 33.3 Percentage distribution of infarct size in 200 fatal first-episode acute myocardial infarction (AMI) cases and in chronic patients. The first column refers to the number of cases. Reproduced with permission from Fineschi et al. (2006).
Table 33.4 Time of evolving infarct necrosis in three different studies. Reproduced with permission from Fineschi et al. (2006).
Table 33.5 Myocarditis classification. Reproduced with permission from JCS Joint Working Group (2011).
Table 33.6 Dallas criteria for the diagnosis of myocarditis. Reproduced with permission from Aretz (1987).
Table 33.7 Myocarditis – classification in relation to type of inflammatory reaction and causal agents. Reproduced with permission from Fineschi et al. (2006).
Table 33.8 Infectious causes of human myocarditis. After Andréoletti et al. (2009).
Table 33.9 Histological age determination of venous thrombosis and embolisms. Reproduced with permission from Fineschi et al. (2009).
Table 33.10 Summary of pathological findings in eight fatal cases of influenza A/H1N1. After Rosen et al. (2010).
Table 33.11 Conditions that may mimic asthma. After Byard (2011).
Table 33.12 Causes, means of diagnosis and characteristics of intracerebral haemorrhage. After Qureshi et al. (2001).
Table 34.1 Efficiency criteria for choosing a biological fluid.
Table 34.2 Postmortem biochemical values in case of alterations in glucose metabolism.
Table 34.3 Postmortem biochemical values in cases of renal failure (insufficiency).
Table 35.1 Live births and infant mortality in Germany from 2001 to 2010. Data from SBD (2011).
Table 35.2 Most frequent causes of death in infants and children in 2010 in Germany. Data from SBD (2011).
Table 35.3 Overview of genetic investigations in sudden infant death syndrome (SIDS) and sudden and unexpected deaths in infants (SUDI) cases.
Table 35.4 Criteria used in the San Diego definition. From Bajanowski et al. (2006), © Springer.
Table 35.5 Risk factors for SIDS. Adjusted odds ratios and 95% confidence intervals (CI) from the CESDY study (Fleming et al. 1996) and the German SIDS study (Vennemann et al. 2005a).
Table 35.6 Relative risk of SIDS depending on sleeping position. Results of the German SIDS study. Reproduced with permission from Vennemann et al. (2005a), © Wiley.
Table 35.7 Relative risks of co-sleeping during previous/last night and infant's age. Results of the German SIDS study (Vennemann et al. 2005a), © Wiley.
Table 35.8 Immunisation as a risk of SIDS. Results from the literature (Vennemann et al. 2007a, 2007b).
Table 35.9 Metabolic diseases as possible cause of sudden and unexpected death in infancy that can be diagnosed by tandem mass spectrometry.
Table 36.1 Main findings during the anogenital examination of children and adolescents and their up-to-date significance.
Table 37.1 Prospective studies of the risk factors for non-accidental head injury (NAHI).
Table 37.2 Retrospective studies of the risk factors for non-accidental head injury (NAHI).
Table 37.3 Symptoms reported to personnel at the primary or secondary hospital of presentation from 106 cases of non-accidental head injury (with definite and probable surety) with the child under the age of 1 year, from a Scottish database.
Table 37.4 Modification of the Glasgow Coma Score for children aged under 5 years (BPNA 2001).
Table 37.5 The main features of non-accidental skeletal injury (NASI).
Table 37.6 Summary of literature on biomechanics studies in non-accidental head injury.
Table 37.7 Differential diagnoses of congenital or acquired pathologies that predispose to individual components of the shaken baby syndrome.
Table 37.8 An overview of outcome of non-accidental head injury from cumulated literature.
Table 37.9 Consequences of different forms of blunt violence. Reproduced with permission from Madea (2007), © Springer.
Table 37.10 Ageing of bruises according to different authors. Reproduced with permission from Hobbs et al. (1993a), © Churchill Livingstone.
Table 37.11 Examinations are decisive from a forensic point of view in order to disprove defensive statements. Reproduced with permission from Madea (2007), © Springer.
Table 37.12 Fractures associated with non-accidental injury. From Wynne (2003); after Hobbes et al. (1999b) and Spevak et al. (1994).
Table 37.13 Radiological findings and possible cause of injuries. Reproduced with permission from Madea (2007), © Springer.
Table 37.14 Healing of fractures. Reproduced with permission from Wynne (2003); after Chapman (1992).
Table 37.15 Differential diagnoses of accidental and non-accidental scaldings. Reproduced with permission from Madea (2007), © Springer.
Table 37.16 Characteristics of accidental and non-accidental contact burns. Reproduced with permission from Madea (2007), © Springer.
Table 37.17 Differential diagnoses of symptoms of child abuse. Reproduced with permission from Madea (2007), © Springer.
Table 37.18 Differential diagnoses of some morphological changes encountered in the abuses child. Reproduced with permission from Pearn (1989); from Oehmichen et al. (2006).
Table 37.19 (a) Differential diagnosis of bruising. Reproduced with permission from Wynne (2003), © Greenwich Medical London.
Table 37.19 (b) Features of haematological disorders that can be confused with non-accidental bruising. From Wynne (2003).
Table 37.20 Poisoning – is it accident, neglect or deliberate?
Table 41.1 Phases of skin wound healing (Singer and Clark 1999) and abrasions (Robertson and Hodge 1972).
Table 41.2 Phases of fracture healing. From DiMaio and DiMaio (2001).
Table 41.3 Differentiation of chronic ulcers. From Takahashi et al. (2004).
Table 41.4 Decubitus ulcer grades: macroscopical and histopathological features. After Shea (1975).
Table 42.1 Typical causes of self-injuries and their morphology.
Table 42.2 Psychological and morphological criteria and characteristics shown in patients or examinees showing self-inflicted injuries.
Table 42.3 Differentiation of self-injuries and injuries done by a third person.
Table 45.1 Fatal toxicity indices (FTIs) for some hypnotics and sedatives in 2008–2010 in Finland. The defined daily dose (DDD) is 7.5 mg for zopiclone, 20 mg for temazepam and 50 mg for oxazepam. Sales are given in DDD (mg) per 1000 inhabitants per day.
Table 46.1 Selected publications showing the influence of ethanol on fatal concentrations of drugs.
Table 46.2 Selected publications showing the influence of drug combinations associated with serotonin toxicity.
Table 47.1 Acute poisoning: clinical features associated with specific poisons.
Table 47.2 Some investigations that are valuable in managing poisoned patients.a
Table 47.3 Some emergency toxicological analyses that may influence the treatment of poisoning.
Table 47.4 Some less urgent toxicological analyses that may influence treatment of poisoning.a
Table 47.5 Some commonly used antidotes.
Table 47.6 Active elimination techniques.
Table 47.7 Sample requirements for general analytical toxicology.
Table 47.8 Advantages and disadvantages of different sample types in analytical toxicology.
Table 47.9 Sample requirements for measurements of metals/trace elements.
Table 47.10 Some factors that may affect interpretation of toxicology results.
Table 47.11 Interpretation of some toxicological analyses that may influence treatment.
Table 47.12 Factors influencing the likelihood of postmortem change in blood poison concentrations.
Table 47.13 Toxidromes: typical signs and symptoms of poisonings.
Table 48.1 Advantages and disadvantages of the most common instrumental techniques used in forensic toxicology.
Table 48.2 Maximum permitted tolerances for relative ion intensities using a range of mass spectrometric techniques.
Table 49.1 Types of stability referred to in current guidelines for bioanalytical method validation and description (Dadgar and Burnett 1995; Nowatzke and Woolf 2007; Peters 2007).
Table 49.2 Prodrugs: examples and bioconversion. After Rautio et al. (2008), © Nature Publishing.
Table 49.3 Possible mechanisms operating on drugs postmortem. Examples modified from Skopp (2004).
Table 49.4 Intrinsic factors and requirements of a urine sample.
Table 49.5 Pre-analytical influences affecting stability of drugs in hair.
Table 51.1 Some physicochemical properties of aliphatic alcohols encountered in forensic and legal medicine.
Table 51.2 Results of an external proficiency test of clinical chemistry laboratories in Sweden with focus on the analysis of certain alcohols and acetone in plasma by gas chromatographic methods.
Table 51.3 List of toxic alcohols and their metabolites often encountered in clinical and forensic toxicology and comments about their occurrence and manifestations of toxicity.
Table 51.4 Examples of elimination rates of ethanol from blood (β) and the apparent distribution volumes (rho factor or Vd) based on results from hundreds of human dosing experiments.
Table 51.5 Approximate concentrations of congener alcohols (mg/L) determined in alcoholic beverages along with their ethanol content as vol%. After Bonte (2000).
Table 51.6 Concentrations of acetone and isopropanol in postmortem blood in diabetic ketoacidosis, alcoholic ketoacidosis and isopropanol intoxication deaths.
Table 51.7 Consequences of inappropriate use of γ-hydroxybutyric acid. Reproduced with permission from Madea and Musshoff (2009), © Deutsches Ärzteblatt, Ärzte-Verlag GmbH.
Table 51.8 Some pharmacokinetic parameters of sedative-hypnotics.
Table 51.9 Elimination half-life, volume of distribution, typical dose, duration of action and action at drug receptor for selected opioids.
Table 51.10 Toxicity of hydrogen sulphide (H2S). From TOXNET NLM HSDB (2013), © US National Library of Medicine.
Table 51.11 Respiratory toxicities of selected gases or solvent vapours and current occupational thresholds. From TOXNET NLM HSDB (2013), © US National Library of Medicine.
Table 51.12 List of common natural poisons and their sources including the botanical names, common English names, the corresponding main toxic compounds and the common detection of these compounds in biological fluids.
Table 51.13 Overview of prohibited substances and methods of doping according to the World Anti-Doping Agency (WADA) Prohibited List of 2011.
Table 52.1 Requirements at different levels of driving behaviour. After Brenner-Hartmann and Berghaus (2007, table B1.2, p. 139), © Ärzte-Verlag, Köln.
Table 52.2 Michon's hierarchical model. Summarised from Owens and Ramaekers (2009).
Table 52.3 Classification system of driving-related performance, behaviour and mood, and corresponding tests and examples. After Schnabel et al. (2010, table 1, pp. 22–3).
Table 52.4 Influencing factors on fitness to drive, driving skills and driving aptitude.
Table 57.1 Odds ratios of THC from various case–control studies: dependence of the results on adjustment variables.
Table 57.2 Selection of determinants affecting the results of an epidemiological study.
Table 57.3 Number of crashes with injured persons as a result of human factors in 2003. Based on statistics from the Federal Office of Statistics, Germany; after Hasse and Schepers (2007).
Table 57.4 Types of ‘driver unfitness’ (see Table 57.3). After Albrecht (2007), © Ärzte-Verlag, Köln.
Table 57.5 Prevalence of use of substance groups in drug-positive drivers. Summarised from Isalberti et al. (2011, p. 4).
Table 57.6 Relative risk level of getting seriously injured or killed (based on ORs of nine European countries) when taking different substances and driving. After Hels et al. (2011, table 33, p. 42).
Table 57.7 Relative risk level of getting seriously injured or killed depending on the blood alcohol concentration (BAC) (based on ORs of nine European countries). After Hels et al. (2011, table 33, p. 42).
Table 58.1 Effects of ethanol on non-tolerant individuals in relation to the their blood alcohol concentration (BAC).
Table 58.2 Different concentration units used to report blood alcohol concentration (BAC) and breath alcohol concentration (BrAC) for legal purposes in different countries.
Table 58.3 Chronological developments in the methods used for quantitative analysis of ethanol in blood for forensic purposes.
Table 58.4 Results of an interlaboratory proficiency test of blood ethanol analysis at specialist forensic laboratories in Nordic countries. Concentrations are reported in mg/g.
Table 58.5 Major developments in the instruments used for breath alcohol analysis, the approximate time period when they appeared and the operating principle for determination of ethanol.
Table 58.6 Statutory limits of blood alcohol concentration (BAC) and breath alcohol concentration (BrAC) and the operational blood : breath ratio of alcohol (BBR) used in some European Union countries.
Table 58.7 Statutory limits of blood alcohol concentration (BAC) and breath alcohol concentration (BrAC) and the operational blood : breath ratio (BBR) used in Germany and the Scandinavian countries.
Table 58.8 Statutory limits of blood alcohol concentration (BAC) and breath alcohol concentration (BrAC) and the operational blood : breath ratio (BBR) used in the USA, Canada, Australia and New Zealand.
Table 58.9 Demographics of people apprehended in Sweden for drunken driving.
Table 58.10 Changes in demographics of drunken drivers in Sweden over time showing mean age, proportion of male to female offenders, and mean blood alcohol concentration (BAC) for the years 2003–2007.
Table 58.11 Demographics of people arrested for drunken driving comparing first arrest offences with recidivists.
Table 58.12 Examples of the types of cognitive and psychomotor tests used to investigate the impairment effects of alcohol on skills necessary for safe driving.
Table 58.13 Relationship between the results of a clinical examination of apprehended drivers by a physician and the degree of alcohol influence, if any. Note that the same physician examined each suspected driver without knowing the individual's blood alcohol concentration (BAC).
Table 59.1 Advantages and disadvantages of the different matrices for roadside drug testing. Summarised from Walsh et al. (2004).
Table 59.2 Recommended scope and analytical cut-offs of toxicological analysis in DUID investigations. Summarised from Musshoff (2011).
Table 59.3 Target analytes and cut-off values for chemical toxicological tests concerning driving ability in Germany (Schubert and Mattern 2009; Brenner-Hartmann et al. 2011).
Table 60.1 Overview of the studies testing hypnotics in the on-the-road driving test. The acute and subchronic effects are indicated in terms of blood alcohol concentration (BAC) required to achieve the same level of impairment.
Table 60.2 Overview of the studies testing anxiolytics in the on-the-road driving test. The acute and subchronic effects are indicated in terms of blood alcohol concentration (BAC) required to achieve the same level of impairment.
Table 60.3 Overview of the studies testing antidepressants in the on-the-road driving test. The acute and subchronic effects are indicated in terms of blood alcohol concentration (BAC) required to achieve the same level of impairment.
Table 60.4 Overview of the studies testing antihistamines in the on-the-road driving test. The acute and subchronic effects are indicated in terms of blood alcohol concentration (BAC) required to achieve the same level of impairment.
Table 61.1 Characteristics of alcohol biomarkers (Brinkmann et al. 2000; Conigrave et al. 2003; Hannuksela et al. 2007; Niemelä 2007; Jones 2008; Liangpunsakul et al. 2010; Pirro et al. 2011).
Table 62.1 Morphological correlations between positions of the body at collision and expected injury patterns. Reproduced with permission from Driever et al. (2002), © Elsevier.
Table 62.2 Morphological correlations between train speeds and injury patterns in case of collision between the rails. Reproduced with permission from Driever et al. (2002), © Elsevier.
Table 63.1 Crime scene processing techniques and DNA.
Table 63.2 Commercially available DNA typing kits.
Table 63.3 Factors influencing polymerase chain reaction (PCR) results.
Table 63.4 Sample calculation for a DNA profile.
Table 63.5 Key quality factors for a DNA database.
Table 63.6 Characteristics and current status of SNP markers.
Table 63.7 Commercially available Y STR typing kits.
Table 63.8 X chromosome typing results in a sibship case.
Table 63.9 Relevant hypotheses in the sibship case.
Table 66.1 Some typical sources of problems concerning medical activity (Tag 2011).
List of Illustrations
Figure 1.1 Constitutio Criminalis Carolina (criminal code of Emperor Charles V). Reproduced from http://commons.wikimedia.org/wiki/File:De_Constitutio_criminalis_Carolina_(1577)_13.jpg (last accessed 12 June 2013).
Figure 1.2 Paolus Zacchia (1584–1659), called the ‘Father of forensic medicine’. Courtesy of the US National Library of Medicine, History of Medicine Division.
Figure 1.3 Title cover of Paulus Zacchias's book Quaestiones medico-legales.
Figure 1.4 Mathieu-Joseph Bonaventura-Orfila (1786–1853).
Figure 1.5 Johann Ludwig Casper (1796–1864), founder of modern forensic medicine in Prussia.
Figure 1.6 Cut-through of the Institute of Forensic Medicine at the University of Berlin (built from 1884 to 1886). The institute served also as a morgue where unidentified deceased people were exhibited for public viewing. At the first floor a man is standing in front of a glass window, behind the window bodies are exhibited in cooling cells. The Paris morgue served as a model for the construction of the morgue in Berlin.
Figure 1.7 Eduard von Hofmann (1837–1887), professor of forensic medicine in Vienna from 1875 to 1887. His time in Vienna is called the golden age of forensic medicine. He published not only a famous textbook and an atlas of forensic medicine, but numerous articles throughout the whole discipline. He had many important pupils who performed outstanding experimental research.
Figure 1.8 Title cover of Eduard von Hofmann's Textbook of Forensic Medicine.
Figure 2.1 Tasks of forensic medicine. As a cross-sectional discipline, it uses the knowledge of numerous different fields of expertise.
Figure 3.1 Exhumation of a single grave, the Philippines.
Figure 3.2 Open air autopsy on a hot summer day, Kosovo.
Figure 3.3 Autopsy teams, Kosovo.
Figure 3.4 Body bags with killed hostages, Colombia.
Figure 3.5 Land mine victim, Burma. He was smuggled out of the country and the photo was taken at a hospital in Thailand.
Figure 3.6 Forced labour, Burma. Villagers are forced to carry heavy weights of cargo over long distances. The painting was made by a survivor.
Figure 3.7 Whipping, Togo. The victim was accused of the theft of two chickens and was whipped to provoke a confession.
Figure 3.8 Close up of scars after cigarette burns.
Figure 5.1 Schema and terms of the agonal period. The agonal period is initiated either by disease or trauma.
Figure 5.2 Older female lying dressed at the bank of a river. Vital signs were missing. Although postmortem changes (lividity, rigor mortis) were missing she was pronounced dead by an emergency physician. The symptom of cold stiffening was probably mixed up with rigor mortis. Cause of death was intoxication with central nervous system depressants.
Figure 5.3 Diagram of agonal period, individual death, supravital period and biological death. The moment of individual death is of medical and legal importance.
Figure 5.4 Flow chart for the diagnosis of brain death. EEG, electroencephalogram. Reproduced with permission from Bundesärztekammer (1998), © Deutsches Ärzteblatt, Ärzte-Verlag GmbH.
Figure 5.5 Brain death checklist. From New York State Department of Health (2005), © New York State Department of Health. (Continued on next page.)
Figure 6.1 International form of medical certificate of cause of death.
Figure 6.2 Types of death. After Leis (1982) and Thieke and Nizze (1988); case examples reproduced with permission from Thieke and Nizze (1988) and Madea (2004).
Figure 6.3 Causes of death, showing the proportion of unnatural causes of death among deaths in Germany 2007. Courtesy of the Federal Statistical Office, Germany (www.destatis.de; last accessed 12 June 2013).
Figure 6.4 Warning colours in suicidal intoxication. (a) Combined suicide by oxydemetonmethyl ingestion and hanging, as evidenced by the blue stain flow from the left side of the mouth and strangulation mark. (b) Intensive blue colour of mouth and lips in a case of suicidal intoxication with solvents.
Figure 7.1 Duration of the supravital period (bottom) compared to the resuscitation period (top). The supravital period after irreversible circulatory arrest exceeds the duration of the resuscitation period after transient ischaemia by far. After Madea (2007), © Springer.
Figure 7.2 Three phases of idiomuscular contraction after mechanical excitation of the muscle; frequency of a positive reaction (y axis) over the postmortem interval (x axis); hpm, hours postmortem. After Dotzauer (1958), © Springer.
Figure 7.3 Typical idiomuscular pad of the biceps brachii muscle. Courtesy of Professor G. Dotzauer.
Figure 7.4 Position of electrodes for examining electrical excitability of facial muscles.
Figure 7.5 Six degrees of positive reaction after stimulation of the orbicularis oculi muscle (see also Table 7.1).
Figure 7.6 Square wave generator for defined stimulation of facial muscles enabling the procurement of the data in Table 7.1 and Fig. 7.7. Producer and supplier: http://j-peschke.homepage.t-online.de (last accessed 17 April 2013).
Figure 7.7 Postmortem lividity. (a) Postmortem lividity in a supine position, pink colour due to storage in a refrigerator. (b) Petechial-like haemorrhages due to capillary ruptures in areas of deep hypostasis (vibices). (c) Zonal segmentation of hypostasis: partly dark blue, partly red. (d) Brownish colour of hypostasis in case of methaemoglobin intoxication. (e) Patterned hypostasis of the back due to the underground. (f) Complete disappearance of lividity on light blunt pressure.
Figure 7.8 Shifting of lividity after turning the body. hpm, hours postmortem. After Patscheider and Hartmann (1993).
Figure 7.9 Due to rigor mortis the lower leg is fixed against gravity (a). Objects in the hand such as branches must not be mixed-up with instantaneous rigor mortis or cadaveric spasm (b).
Figure 7.10 Re-establishment of rigor mortis after breaking. If rigor is broken during the development of rigor mortis (at D or E), it will re-establish at a lower level (at D1 or E1). If rigor is broken (e.g. at F) after it has fully developed (B) it will not re-establish at all. After Madea (2007), © Springer.
Figure 7.11 Gooseflesh of the right forearm due to rigidity of the smooth musculi arrectores pilorum.
Figure 7.12 Sigmoidal shape of the cooling curve which is best described by Marshall and Hoare's (1962) two-exponential term. The quotient (Tr − Ta)/(T0 − Ta) is a good measure of the progress of cooling. If this quotient Q is <0.3, only a minimum interval for the time since death should be given. T0 = rectal temperature at death (T = 0), Tr = rectal temperature at any time, Ta = ambient temperature. hpm, hours postmortem.
Figure 7.13 Temperature–time of death nomogram for ambient temperatures up to 23°C. At the scene of death, for instance, a rectal temperature of 27°C at an ambient temperature of 15°C were measured. Firstly, the point of the scale of the measured rectal temperature and ambient temperature have to be connected by a straight line (yellow) which crosses the diagonal of the nomogram at a specific point. Secondly, a second straight line has to be drawn passing through the centre of the circle (below left of the nomogram) and the intersection of the first line and the diagonal (red line). The second line crosses the semicircles for different body masses. The time since death (in this case for 70 kg body mass) can be read at the intersection of the semi-circle of the given body mass. The intersection gives the mean time since death, the intersection with the outer circle the 95% limits of confidence, which may be higher if corrective factors have to be used.
Figure 7.14 Temperature–time of death nomogram for ambient temperatures above 23°C.
Figure 7.15 Triangular dark discoloration of cornea (‘tache noir’).
Figure 7.16 (a–c) Bloating of tissues, discoloration and putrefactive blisters of the skin.
Figure 7.17 Venous marbling.
Figure 7.18 Hands of a homicide victim 2 years after murder. The body was wrapped into several plastic bags. Although epidermis is completely lost a dactyloscopic indentification was possible.
Figure 7.19 (a) Decomposition with patches of fungus on the face. (b) Advanced decomposition after exhumation with fungus patches on the skin.
Figure 7.20 Advanced skeletonisation of the skull after 1 week lying on the surface in the wood in summer.
Figure 7.21 Gnawing marks of the epidermis of the hands by mice.
Figure 7.22 Mummification of a body in a fixed position. The man was lying on the couch of his apartment for half a year (the autumn and winter) after death with the doors and windows open.
Figure 7.23 Mummificaiton of the whole foot sole within 3 days after death.
Figure 7.24 Saponification. (a) Soft tissues of the thighs were converted into hard shells of adipocire with the long bones hanging loosely. (b) Saponification of the head. (c) The leg of a newborn child, with saponification, after lying in flowing water for several months, the outer shape of the legs was preserved; the chalk-like brittle mass, which looks like a stiff tube, contains loose bones. The muscles are missing. (d) The texture of the fat nodules in the subcutaneous fatty tissue was fixed by adipocere formation (‘état mammelloné’).
Figure 7.25 Main principle of the determination of the time since death (calculation from a measured value along a curve back to the initial value).
Figure 7.26 Mean values (black bars) and variations of different time of death-dependent criteria. Red: lividity (Liv.); blue: mechanical excitability of skeletal muscle; yellow: electrical excitability (Electr. exc.); green: rigor mortis (Rig.); orange: pharmacological excitability (Ch. exc.). orb., orbicularis.
Figure 7.27 Integrating chart for casework at a scene of crime.
Figure 7.28 Integrating chart for casework filled in at a scene of crime as an example.
Figure 7.29 Integrating chart with contradictory results of death time estimation based on body cooling (nomogram), rigor mortis and electrical excitability (case of fatal hypothermia).
Figure 7.30 Combined application of the temperature-based nomogram and the electrical excitability for determining the time since death. Boxes show death time estimation by the nomogram method (lower and upper 95% limits of confidence). The > and < signs indicate death time estimation based on the degree of electrical excitability. For instance, degree III positive (case 15) not only provides the information that the time since death is less than 13 hours postmortem but is also degree IV negative, therefore the time since death is >3 hours postmortem. Especially during the time period from 3 to 8 hours postmortem, combining electrical excitability with the nomogram method allows more precise death time estimation than using one method alone. The real time since death was always within the calculated time since death.
Figure 7.31 Relation between gastric volume and a mixed meal in per cent of ingested volume and time after ingestion with regression line, 90% and 98% limits of confidence. Reproduced with permission from Tröger et al. (1987), © Schmidt-Römhild, Lübeck.
Figure 7.32 Visitation of several interacting insect groups in different stages of decomposition. 1, fresh (a few hours after death); 2, active decay (2 weeks after death); 3, advanced decay (3 weeks after death); 4, advanced decay (2 months after death); 5, dry or skeletonised (2 years after death). See text for more explanation.
Figure 7.33 Blow flies on carcass: (a) Extended proboscis of blow fly. (b) Extended ovipositor of blow fly.
Figure 7.34 Blow flies forming aggregations on carcass to oviposit.
Figure 7.35 Case 1: (a, b) state of the corpse, (c) open abdominal cavity, (d) close-up inside abdominal cavity showing hundreds of larvae and pupae of Megaselia scalaris.
Figure 7.36 Case 2: (a) area where the torso of the body was found, (b) torso of the body packed in a plastic bag with several fly larvae attached.
Figure 7.37 Scleral desiccation. The area of the sclera exposed to air has dried out, leaving a brownish-reddish band-like zone that should not be confused with scleral haemorrhage.
Figure 7.38 (a) Distension of the penis and scrotum in a putrefied body. (b) Brownish-blackish appearance of the skin that may mask traumatic injuries such as current marks, defensive injuries or puncture marks. (c) Postmortem protrusion of the tongue due to putrefactive gas formation and purging of putrefactive fluid from the nostrils. (d) Postmortem purging of putrefactive fluid from the mouth. (e) Purging of putrefactive fluid from the mouth and nostrils that should not be misinterpreted as effusion of blood due to a violent mode of death. (f) Putrefactive fluid-filled skin blisters. (g) Skin slippage in a putrefied body. (h) Venous marbling. (i) Venous marbling that may appear as bruising to the inexperienced. (j) Venous marbling.
Figure 7.39 (a) Washer-woman's skin in a body recovered from water. (b) Postmortem injury following a cut from a ship's propeller. (c) Wound of postmortem origin in a body recovered from water. Wounds, even those acquired antemortem, appear bloodless when the body has spent a considerable time span in water. (d) Postmortem floating injuries on the face. (e) Postmortem floating injuries on the face. (f) Postmortem floating injuries on the back of the hand. (g) Postmortem injuries caused by crustaceans in a body recovered from water. (h) Postmortem injuries caused by crustaceans. These wounds are typically oval to round, crater-like and of varying size. (i) Facial postmortem injuries caused by sea lice (Natatolana woodjonesi). Courtesy of Professor Jules Kieser, Otago, New Zealand. (j) Auricular postmortem defects caused by sea lice (N. woodjonesi). Courtesy of Professor Jules Kieser, Otago, New Zealand.
Figure 7.40 Adipocere formation in a body recovered from water.
Figure 7.41 (a) External bevelling of the calvarium in a charred body. This is a pure postmortem artefact. Note that the excavation of the outer table of the cranium shows no charring or soot deposits in contrast to the surrounding parts of the occipital bone, thus indicating that the occipital defect occurred postmortem during the postmortem cooling process. (b) Postmortem skin splitting in a burned body.
Figure 7.42 (a) Postmortem facial injuries inflicted postmortem by rodents. (b) Postmortem injuries inflicted postmortem by rodents. The wound margins are finely serrated and show irregular edges. (c) Postmortem injuries inflicted postmortem by rodents. (d) Postmortem defects on the forearm inflicted postmortem by rodents. (e) Postmortem injuries inflicted postmortem by a domestic dog. (f) Postmortem injuries inflicted postmortem by a domestic dog. (g) Claw-induced linear scratch-type abrasions in the vicinity of the damaged skin areas due to postmortem animal interference by a domestic dog. (h) Postmortem skin lesions caused by ants.
Figure 7.43 (a) Postmortem skin lesions caused by cockroaches. (b) Pseudoligature mark due to contact blanching of livor mortis. (c) Vibices in livor mortis. (d) Postmortem skin injury with the typical yellowish-brownish to golden, shiny appearance. (e) Leaking out of gastric juice and bile postmortem. (f) Skin lesions caused by external cardiopulmonary resuscitation. (g) Defibrillation marks.
Figure 7.44 (a) Rib fractures following unsuccessful resuscitation measures. (b) Rupture of the left atrium of the heart following unsuccessful resuscitation measures. (c) Pericardial tamponade. (d) Liver ruptures following forceful resuscitation procedures.
Figure 7.45 Gastric air insufflation due to incorrect intubation.
Figure 8.1 (a, b) Contemporary cremation of a body in different stages in the primary incinerator. Courtesy of Patrik Budenz.
Figure 8.2 Examination room at a crematory; findings at external examination before cremation must apply to the death certification.
Figure 9.1 The autopsy room showing the unitary table design combining evisceration and dissection areas, and spacious and abundant daylight from high windows (not shown).
Figure 9.2 Y-shaped incision for evisceration. Courtesy of T. Hansen.
Figure 9.3 Spinal column opened to reveal metastases or fractures. Courtesy of T. Hansen.
Figure 9.4 Normal postmortem computed tomography (PMCT) findings. (a) Axial PMCT image of the head showing high attenuation of the dorsal part of the sagittal sinus (arrow). This finding is normal in the postmortem setting and should not be confused with the antemortem ‘delta’ sign, which suggests thrombosis of the sinus. A low attenuation area on the right hemisphere is also seen (encircled, old brain infarction). (b) Axial PMCT image of the thorax, at the height of the arteria pulmonalis. Notice the hyperdense structure which overlaps both lung arteries (marked red in the magnified segment). The differential diagnosis between postmortem clot and true pulmonary embolism is impossible without additional modalities (postmortem magnetic resonance imaging, PMCT biopsy). (c, d) Axial PMCT images of the lungs. Dorsal (c, black arrows) and frontal (d, white arrows) opacities due to internal livor mortis indicate the position of the deceased (supine and prone, respectively).
Figure 9.5 Decomposition (PMCT, coronary view). Notice the gas in the soft tissues, as well as the organs and vessels. The intestines are inflated and there are surface defects on the right supraclavicular area.
Figure 9.6 Foreign objects and fractures on PMCT. (a, b) Gunshot injury to the head. (a) Oblique PMCT image of the head showing the entry wound on the right parietal bone, typically with greater inner table defect than that of the outer table. Osseous fragments penetrate the brain parenchyma. The end position of the projectile is left to the midline. (b) 3D reconstruction of the head, view from the left oblique side. Part of the facial structures have been removed. The entry wound defect, as well as the position of the projectile, are exactly depicted. (c, d) Fatality after fall from height. (c) Axial PMCT image of the second vertebrae. The arrows indicate fractures of the vertebral arch, which are not easily demonstrated during autopsy. (d) 3D reconstruction of the head. The fracture pattern can be shown prior to removing the scalp, as this can lead to fragment dislocation.
Figure 9.7 Natural cause of death. (a) Axial PMCT image showing a pericardial tamponade. At a higher level (magnified inset) an intima flap of the aorta is suspected (arrows). (b) Cardiac postmortem magnetic resonance image (T2-weighted sequence) of the same case. The aortic dissection is now better visualised (arrows). Aortic dissection and rupture caused the pericardial tamponade.
Figure 9.8 Postmortem computed tomography angiography. Administration of the contrast medium mixture through the right femoral vessels (notice the parallel-lying cannulas) produces a 3D volume rendering of the arterial tree. The arrow points out a bypass vessel.
Figure 9.9 Surface injury illustrations with different modalities. (a) 3D surface reconstruction from a PMCT scan dataset. (b) High resolution surface scanning with an optical 3D scanner (ATOS III, Rev. 01, Braunschweig, Germany). (c) High resolution surface scanning with additional colour information (retrieved from a digital single-lens reflex camera).
Figure 12.1 Skeletonised body of a woman found on a rubbish site 1.5 years after her death. The skeleton is still in anatomical connection and dressed; the cranium is fragmented.
Figure 12.2 Example of dispersion of bone segments in a wooded area affected by extensive animal colonization and a steep slope: the movement of bone remains was due both to gravity and animal activity.
Figure 12.3 Example of a charred body found in a car. An informant reported that the hands were cut off after death in this victim of an execution by organized crime. (a) The body showed the absence of the distal portion of both the upper limbs. (b) However, a search for bone fragments on the floor of the car revealed two fragments of the right and left radius (indicated by red circles) which did not show signs of cut marks. This particular region of the wrist would very likely have been cut or maimed if the hands had been cut off. (c) The bones found from the first recovery of the body (in blue) and the second search of bone fragments in the car (in red).
Figure 12.4 The recovery procedure of a buried body: (a) removal of superficial layers of the soil; (b) exposure of the skeleton; (c) cleaning of the surrounding area with respect to the anatomical position and stratigraphic characteristics of the soil; and (d) complete exposure of the burial.
Figure 12.5 Comparison between a thin, non-decalcified section of a recent bone (a) and an archaeological one (b) affected by tunnelling, degradation and invasion of fungi (40×).
Figure 12.6 The luminol test. (a) Luminol testing on a bone sample in a forensic case with a slight reaction. (b) A positive control with human blood.
Figure 12.7 Osteon assessment for the diagnosis of species. Specific software can provide an easy measurement of osteon parameters.
Figure 12.8 Comparison of a male pelvis (left) and female pelvis (right); the red arrow shows the position of the ventral arc in the female pubis. The subpubic angle has an upside down V shape in males and a wider U shape in females.
Figure 12.9 Comparison of a female cranium (left) and male cranium (right). Arrows; blue, glabella; red, superciliar edge; brown, zygomatic arch of the temporal bone; orange, mastoid process; green, gonial eversion; light blue, nucal crest.
Figure 12.10 (a) Age of fusion of the main epiphyses. (b) Phases of fusion of the vertebral structure (upper: newborn; middle: 2 years; lower: 10 years).
Figure 12.11 Stages of the Suchey–Brooks method: I, 19.4 years in females (SD 2.6) and 18.5 in males (SD 2.1); II, 25 years in females (SD 4.9) and 23.4 in males (SD 3.6); III, 30.7 years in females (SD 8.1) and 28.7 in males (SD 6.5); IV, 38.2 years in females (SD 10.9) and 35.2 in males (SD 9.4); V, 48.1 years in females (SD 14.6) and 45.6 in males (SD 10.4); VI, 60.0 years in females (SD 12.4) and 61.2 in males (SD 12.2).
Figure 12.12 Stages of the Iscan method: 0, <16 years in males and <13 in females; I, 17–19 years in males and 14–15 in females; II: 20–23 years in males and 16–19 in females; III: 24–28 years in males and 20–24 in females; IV: 26–32 years in males and 24–32 in females; V: 33–42 years in males and 33–46 in females; VI: 43–55 years in males and 43–58 in females; VII: 54–64 years in males and 59–71 in females; VIII: >65 years in males and >70 in females.
Figure 12.13 Stages of the Lovejoy method: I: 20–24 years; II: 25–29 years; III: 30–34 years; IV: 35–39 years; V: 40–44 years; VI: 45–49 years; VII: 50–59 years; VIII: 60+ years.
Figure 12.14 Root transparency (light blue line) in a mono-radicular tooth visible on a light box.
Figure 12.15 The left side shows the points of evaluation of cranial sutures. The right side shows the classification of fusion from (a), with 0 points, to (d), with 3 points. The sum of all the scores recorded from the 10 points gives the age estimation according to specific tables.
Figure 12.16 Crania belonging to the three main racial groups: (a) Caucasoid cranium, (b) Negroid cranium and (c) Mongolid cranium.
Figure 12.17 Femoral prothesis: it may show the code of the specimen, and therefore be useful for a personal identification.
Figure 12.18 Examples of bone calluses on the ribs at different degrees of healing.
Figure 12.19 Osteophytosis in two arthrosic vertebrae.
Figure 12.20 Sacroiliac anchylosis showing sign of arthrosis or autoimmune pathology.
Figure 12.21 (a) Deformation of the femur due to rickets (vitamin A deficiency). (b) Cribra orbitalia related to anaemia due to a lack of iron.
Figure 12.22 Different phases of facial reconstruction. The hair was modelled according to the residues of hair found on the decomposing cadaver. Courtesy of Dr Davide Porta, University of Milano.
Figure 12.23 Facial reconstruction in a forensic case: details of the smiling version of the reconstruction, with the original dental profile of the unknown decedent.
Figure 13.1 Disaster classification based upon availability of victim manifest.
Figure 13.2 Cover page of the Interpol disaster victim identification (DVI) yellow form for antemortem information.
Figure 13.3 Cover page of the Interpol disaster victim identification (DVI) pink form for postmortem information.
Figure 13.4 Disaster victim identification workflow with computed tomography (CT) scan; DNA sample collection would take place during forensic pathology.
Figure 16.1 Continuum due to stress with stretch εyy (A → A′, B→ B′), crosswise contraction εzz and shearing (α + β = γyz).
Figure 16.2 (a–e) Separation of coherence due to tension, pressure and shear.
Figure 16.3 Development of a bending fracture. (a) Development of longitudinal tension opposite the location of the primary force. (b) Development of a first (small) rupture with a simultaneous change of the stress field. (c) Complete Messerer fracture. (d) Messerer fracture of the tibia.
Figure 16.4 Shell fractures (e.g. globe fracture). (a) Increase of the latitudinal lines with the simultaneous development of tensile stress. (b) Partial aspect: longitudinal bursting fracture. (c) Partial aspect: bending fracture along the latitudinal line. (d) Pattern of a globe fracture in principle.
Figure 16.5 Pressure causing deformation and separation of coherence. (a) Pressure causing deformation of an elastic disc provoking stress within the material. (b) Traumatogenesis of a combined ‘crush–tear injury’. (c) Traumatogenesis of a compression fracture.
Figure 17.1 Percentage of deaths related to time and causation.
Figure 17.2 Three-dimensional reconstruction of postmortem computed tomography (CT) image of a fatal, disruptive shotgun injury to the head.
Figure 17.3 The tongue, pharynx and laryngeal structures showing the effects of inhalation of hot gases.
Figure 17.4 A bleeding varicosity resulted in blood spatter which was then modified by a household pet to result in extensive blood spatter throughout the scene.
