Knights, Simpson’s Forensic Medicine, 13 th ed., Arnolds, 2008.

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Presentation transcript:

Knights, Simpson’s Forensic Medicine, 13 th ed., Arnolds, 2008.

 To learn the concept of sudden death from forensic and clinical point of views.  To learn how to estimate unnatural causes of death  To learn the natural causes of death  To learn when a death certificate can be issued  To learn how to diagnose death  To learn how to estimate time of death

= Brainstem death Indonesian Medical Association (SK PB IDI No. 336/PB/A.4/1988) Do we need EEG to diagnose death??

Death is a process not an event, at the time of death there is a progression from clinical death to brain death, to somatic death, to cellular death. 1. Cardiac death 2. Clinical death 3. Somatic death 4. Brain death 5. Cellular death So, what is sudden death?

WHO : someone who dies within 24 hours of symptoms appearing. Forensics: different meaning Manner of death Mechanism of death

NaturalUnnatural Suicidal Homicidal Accidental

Death certificate Once the fact of death is established, a death certificate is issued unless a post-mortem examination is requested.

Heart attacks Strokes Fatal diseases Pneumonia SIDS Old age Cancer etc Typically a person who dies of natural causes has been under a doctors care. However, some times a death is made to look like it is from natural causes.

Cardiovascular causes Extra-cardiac causes

Coronary artery disease 50% of cardiovascular deaths Above 30 y.o. Coronary insufficiency  Narrowing of the lumen  chronic ischaemia Hypoxic myocardium is electrically unstable No need for severe ischaemia for ventricle fibrillation. Complication of atheroma  stenosis Myocardial infarction Cardiac tamponade Old women 2 or 3 days after the onset of infarction Hypertensive Heart Disease & Aortic stenosis Left ventricular hypertrophy  size

Within seconds of coronary occlusion  PO 4 hydrolyzed  pH  [K+]  for 10’  Resting membrane potential   Voltage difference btw resting membrane potential and the threshold potential  speeding of conduction  Inhomogeneous conduction, slowing, block at the lateral margin of the ischemic zone; endocardial surface between the subendocardium, midendocardium, and subepicardium;  Conduction block  Initial shortening of refractory period  lengthening of the period  Reentrant ventricular arrhythmias

 Aneurysm  Congenital or family history  Young woman  dd/ - Complication of pregnancy - Pulmonary embolism  History of internal pressure (during delivery, high pressure cough, fall)  Mechanism: cathecolamine release.

 Cerebral haemorrhage  Cerebral thrombosis and infarction

Infarct  injury  [K+] extracell   nerotransmitter out, glutamic acid, aspartic acid  Ca++ entering neuron  [K+] extracell  protease activation  membrane & cytosceleton destruction  Phospholipase C, aracidonic acid & prostaglandin  radicals  vascular & BBB destruction  edema  Cause of death - Transtentorial herniation 48%

 Vascular causes  thromboemboli - Deep vein thrombosis following skeletal trauma (fracture), operation, immobility or bed rest)  Massive hemoptysis  Fulminating chest infections

 Perforation of peptic ulcer - Acute pancreatitis - Severe bleeding

Caution for cases involving woman in childbearing age !  Ruptured ectopic gestation  Abortion - Vagal shock, haemorrhage, infection

Often for ‘no obvious’ reasons. Epileptic patient : - Accident - Asphyxia Asthmatic patient: - Even no status asthmaticus nor severe periode - Over-use of adrenergic drugs, especially by inhaler

Clinical examination, to confirm one or more of the following findings: Prolonged auscultation of the precordial  negative Feeling the radial, or the carotid pulse  negative Other signs of stoppage of circulation include an un- recordable arterial blood pressure, and a flat ECG 1. Complete absence of light reflexes in the pupils 2. Cessation of respiration 3. Insensibility and absent sensory responses to stimuli 4. Loss of nerve reflexes and flat EEG. 5. Ophthalmoscopic examination of retinal vessels, shows segmentation of the blood within them

The cause of death can only be established by a physician in: 1. Patient admitted to ER, or 2. Hospitalized patient, or 3. Autopsy (forensic or clinical autopsy)

Time of Death Can estimate time of death from: early changes after death (thanatology) insect action (forensic entomology) stomach contents (stage of digestion) last known activity (last sighting, newspaper/mail) normal postmortem changes

Early Changes After Death Can estimate time of death from: Rigor mortis Post mortem hypostasis Body temperature (algor mortis) estimate: [98.6 oF – rectal temp]/1.5

Time since death: Change observed 1-2 hours: Early signs of lividity. 2-5 hours: Clear signs of lividity throughout body. 5-7 hours: Rigor mortis begins in face hours: Rigor mortis established throughout the body, extending to arms and legs 12 hours: Body has cooled to about 25 o C internally hours:.....Body has cooled to surrounding temperature. 24 hours: Rigor mortis begins to disappear from the body in roughly the same order as it appeared. 36 hours: Rigor mortis has completely disappeared. 48 hours: Body discolouration shows that decomposition is beginning.