Coroners Autopsy

Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003

The Coroner’s Autopsy from the Book by Bernard Knight, 1983, Churchill Livingstone, Edinburgh, NY

Preface: The Coroner’s Rules on PM Examination: • done A.S.A.P. • done by a pathologist with lab. Facilities • not a pathologist of the hospital where patient dies if: • pathologist not willing • conduct of hospital staff is in question • relatives request so Ch.1: Medicolegal Autopsy Done on behalf of the community which wishes to exclude any criminal or civil responsibility for a death which is unnatural, sudden, unexpected or otherwise obscure. Legal Authority Requesting Autopsy: • Anglo-Saxon Legal code: e.g. coroner & some American states Lawyer +/ Dr appointed by government. The Registrar is legally bound to report 1. unidentified body 2. no Dr attended during last illness / Dr did not see within 14 days prior to death 3. suicide 4. homicide 5. sudden unexpected death or suspicious circumstances 6. alcohol, drugs and poisons related 7. domestic accidents 8. transportation accidents 9. industrial accidents / diseases 10. death during operation / before recovery from anaesthetic 11. allegations of negligence 12. infant deaths (except hospital deaths where cause is confidently known) 13. abortion-related 14. cause of death unknown 15. death in custody The coroner may decide: • not to hold an autopsy à pink “Form A” à referred back to Dr for certification • to hold an autopsy: • natural causes à “Form B” à referred to Registrar for disposal • not “” “” à INQUEST: • natural causes • industrial disease • accidental death • misadventure • suicide • unlawful killing à refer to D.P.P. • open verdict • Code Napoleon: e.g. Procurator Fiscal & European continent The PF is responsible for instigating criminal proceedings and is thus only concerned with excluding a criminal aspect to the death rather than establishing non-criminal causes. Hence, medico-legal autopsy rate is lower in Scotland (25% of reported cases) cf. England (95%). • Medical Examiner • medically qualified official appointee of the administration (USA) • decides whether a death is under his jurisdiction and performs PM • assigns category (suicide etc.) and notifies the DA if criminal

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Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003

Ch.2: The Autopsy Report • Identification of the body and persons present. • May need to use the First Schedule report sheet (but a thorough PM often covers the same ground) • Give a reasonable interpretation of findings and correct cause of death sequence • State ‘unascertainable’ where no reasonable cause can be found Ch.3: The Pathology of Sudden Death CARDIAC: • Coronary artery disease • types of coronary occlusion (fig 3.1) • common sites of coronary occlusion (fig 3.3.) • Myocardial Infarction macro (regional and, to a lesser degree, subendocardial): • 12 - 24hr Nil • 24hr+ yellow/brown pallor (oedema) & lack-lustre • day 2 ‘tigroid’ haemorrhagic/bloodlake streaks & red margin begins • day2-week1 streaks dissappear, myomalacia cordis • week1-2 central gelatinous transformation • week2 fibrosis commences • 2-3 months complete fibrosis with periph. zone of continuing infarction • Myocardial Infarction micro: • 12hr myocyte cloudy swelling (eosinophilia (green filter) & granularity) • 12-24hr more eosin., angulated wavy fibres with pinching • Days: granular break-up of striations (PTAH) with clumping into contraction bands (‘chinese writing’) & loss of nuclei • 2d+ variable leukocyte infiltration • 1wk disintegration of myocytes and granulation tissue • 3-4wk fibroblastic infiltration • 3-6 months avascular collagenous tissue • Subendocardial less necrosis, more fibrosis. Enz à large midzonal area. • Myocardial Infarction: complications: aneurysms are not a source of rupture • ‘Milk spot’ = superficial (friction) fibrosis with no underlying muscle damage. • Hypertensive heart disease (500-600g cf. 360-380) • usually with marked pulmonary oedema • midzonal enyme defect as for subendo MI (due to vasc supply pattern) • Aortic valve disease (hypertroph, decr. aortic root pressure, calcific distortion block sinus entrance) • Cardiomyopathies: • Congestive (globular, all 4, endstage viral, toxins (e.g. etOH with steatosis and mitochondrial swelling), autoimmune d/dg haemochromatosis, beriberi acromegaly, Pompe’s) • Hypertrophic (400-700g, 30% familial, localised, myofibre dissarray, nuclear anomalies, fibrosis) • Restrictive: • EMF (temeperate, eosinophilia(MBP), inflow tracts, papillae+chordae) • EFE (infants, avasc fibrosis, diffuse Lt. atrium & vent, oblit trabec) • (d/dg carcinoid synd: 5-HT subendoc fibrosis on Rt (GIT) or Lt (lung)) • Myocarditis ARTERIAL: • Aortic aneurysm • Atheromatous: Rupture commoner in cold weather. Rare in asc./arch à syphilis • Dissection: Frequently initiates through a patch of intimal atheroma but there is no association between medial necrosis and atherosclerosis. • Syphilitic: Irreg. medial translucency & tree bark intima

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Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003 • Pulmonary embolism • Venous thrombosis assoc.d with trauma, immobility, debilitating illness, cancer, other thromboses, oestrogens and age. • Prob. unsafe to relate a PE to an injury if it was > 1 month beforehand • Embolus or PM clot: Emb. is firmer, paler and not a cast of the vessel. Stratifiacation of the fibrin cannot happen in a PM clot. • If the emb. is too small to be seen at the cut end of the main pulm artery at the hilum of the lung, it is unlikely to be the primary cause of death unless there is other severe debility. • In true thrombosis the cut ends of the vessels show protruding thrombi / emb. • Dating thrombus: • take section from junction of vessel wall and thrombus • endothelial bud proliferation begins on the second day • first appearance of h’siderin occurs on the eighth day (lasts 1yr) CNS: • Cerebral haemorrhage: Most common site is anterior external capsule from Charcot’s ‘artery of cerebral haemorrhage’ (lenticulostriate branches of mid. cereb. art. in ant. perf. substance). H’ge extends to involve the internal capsule à stroke. • Cerebral thrombosis & infarction: • Subarachnoid haemorrhage: In sudden death in women of child-bearing age consider a complication of preg., a thromboembolus or a SAH. No aneurysm in 25% (either a tiny aneurysm is destroyed or the elastocollagenous defect was present without dilatation) • Epilepsy: Always examine the tongue, but may die without fitting (?abn. brain activity). RESPIRATORY SYSTEM: • Asthma: Sudden deaths need not be in status asthmaticus or even an acute attack. • Haemoptysis: TB & tumours • Fulminating pneumonias: Aspiration bronchop. inflammatory foci may resemble a bunch of grapes. The presence of food etc in the airways is doubtful without parench. reaction. GASTROINTESTINAL: • Bleeds from mouth/pharynx ops • Acute gastric erosions may give rise to more extensive bleeding than their appearance may suggest. They are an indicator of hypothermia, head injury, intracerebral lesions and Virchow’s autonomically mediated triad (erosions, subendocardial h’ge, pulm. oedema). If there is no black film at the base then a lacklustre patch is a amarker for a gastric erosion. • Mesenteric infarction: presence of thrombus is more important than degree of atheromatous narrowing hence may cut vessels longitudinally at PM. • Strangulated hernia • Perforation: peptic ulcer (chemical peritonitis), diverticulum/cancer (faecal peritonitis) URINARY: Rarely the primary cause of a sudden death. FEMALE GENITAL TRACT: • ectopic pregnancy • abortion • cardiac arrest due to sudden stimulation of the autonomic NS (cervix) in a patient who is highly apprehensive and tense. • infection including Cl.perfringens • local damage and haemorrhage • air embolism (Higginson syringe) • At PM remove the genital tract and anorectum intact. • pregnancy & childbirth • The C.E. into Maternal Deaths and the PM as a form of substandard care • Look for DIC, gram -ve septicaemia and amniotic fluid embolism (squames, lanugo, vernix, mucin and bile - Lendrum’s phloxine-tartrazine alcian green). • Anaesthetic deaths.

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Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003

Ch.4: Deaths in Infancy and Childhood STILL-BIRTHS & INFANTICIDE A dead-born died in utero whereas a still-born was alive until parturition began. Legally a separate existence means there were life signs (breathing/feeding/moving/crying) after the body (not cord/plac.) had completely left the mother. This implies the potential for homicide (infanticide if mother was in disturbed state of mind). Live-births show life signs when only even partly extruded from the birth canal. The crime of abortion cannot be invoked after the onset of labour and infanticide cannot be committed unless completely extruded - this led to the practice of child-destruction which became criminalised in the Infant Life Act of 1929. If a macerated body is found, live-birth cannot be proved hence concealment of birth is the only charge available. The pathologist may attempt to distinguish live-birth from still-birth as follows: • any maceration makes this impossible • any doubt should be given to the mother • food in the stomach • a vital reaction to the cord e.g. inflammatory reddening in surrounding skin (day 2) • respiration: • the floatation test is of no value • fill chest, pink, spongy & crepitant • histology not useful unless ‘no-touch’ fixed - even then not definite THE BATTERED CHILD SYNDROME • subdural haemorrhage with fractured long bones • the bluntness of the injury may not produce laceration (haematoma and fracture are common) • ruptured abdominal viscus (duodenum, mesentery, liver) • burns or asphyxia • injury to eyes or mouth (e.g. lip laceration from contact with teeth) • bruises of different ages (bruises are very uncommon in preambulatory babies) • fetogram shows raised periosteal calcification and chipped epiphyses around large joints S.I.D.S. • usually in first half of day - evening deaths should be scrutinised even more carefully • usually in sleep and rarely observed • The PM • there are no skin petichiae or conjunctival haemorrhages • abundant intra-alveolar siderophages may suggest imposed upper airway obstruction • purpose is to exclude trauma / natural disease • pathologist should contact those involved in the baby’s care (GP, paed., HV) before diagn. SIDS • babies with old injuries are excluded from the SIDS category even when these did not cause death • atypical deaths should not be called SIDS, and are the cause of death given as ‘unascertained’

Ch.5: Deaths associated with Surgical Procedures and Anaesthesia • Do PM without delay: leaking suture lines at PM may be due to autolysis • Full history is important • Surgeon +/ anaesthetist should be present to explain findings / sequence of events • Carefully worded cause of death CRITERIA FOR REPORTING SUCH DEATHS • during op • within 24hr of op or full recovery from anaesthetic • would this patient have died when they did if no op/anaesth? • was death due to disease / injury for which op was performed? • “” “” “” “” other than that for which “”? • was op / anaesth. vital to save life? • was there defective op/ anaesth. technique? If so surgeon / anaesthetist should be called to explain findings, else tissues / organs should be saved for later examination. • if not reported, the op/anesth. should nowhere be mentioned on the death certificate

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Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003

DEATHS ASSOCIATED WITH ANAESTHESIA 1. Those occurring under anaesthesia but not related to the anaesthetic a) due to the injury / disease operated for (e.g. ruptured aortic aneurysm) b) due to a disease, known beforehand, which made the person ‘at risk’ from anaesthesia c) due to such a disease unknown beforehand d) due to surgical shock / exhaustion or a surgical accident 2. Those due to anaesthetic agents or mode of administration a) cardiac arrest. Any form of irritation of the respiratory tract or any surgical manipulation while the patient is ‘light’ may cause a neurogenic cardiac arrest (the ANS is less depressed that other parts of the nervous system). Inexperienced anaesthetists have a higher such complication rate due to failure to maintain the anaesthesia at a level commensurate with the stage of the procedure being caried out. b) respiratory failure. The above vagal sensitivity is increased by hypoxia. The presence of gastric contents in the airways is seen in 25% of all autopsies and is agonal or due to PM manipulation. c) physical faults e.g. explosions due to static, wrong pipe connections, electric shock, etc. Local anaesthetic hazards: overdosage of the agent or of the vasoconstrictors Spinal or epi-dural: diffusion upwards to vital centres / permanent paralysis from contaminants. Malignant hyperpyrexia: AD, high CPK levels, halogenated agents/suxamethonium, PM à ±DIC

Ch.6: Industrial Injuries and Diseases INDUSTRIAL INJURIES • the presence of alcohol may reduce the liability of the employer • list external lesions and their extent • describe internal signs of trauma • evaluate the previous state of health • give an opinion on the mechanism of death COAL-WORKER’S PNEUMOCONIOSIS (CWP) • compensation if death caused by, contributed to or accelerated by the disease • it may be difficult to assess the relative contributions of pneumoconiosis and chronic infective lung disease, however if a full description is given together with appropriate histology and retained material then the decision can be left to the specialists who are members of the Pneumoconiosis Medical Panel of the DoH. • Both lungs should be retained for PMP examination. The least abnormal should be inflated. The other should be cut at PM • describe any emphysema • grade the amount of dust present (foci may be soft or palpable): • i. dust-free • ii. slight diffuse pigmentation • iii. sparse dust foci (≥1cm apart) • iv. moderate dust foci (>1 per cm) • v. numerous dust foci • nodules (≤3mm, 3-20=’infective nodules’) • PMF (>20mm) are the lesions accepted as a cause or contribution to death • TB • pneumonia • pulm. vessels (inc. thrombosis which may be very severe) • pulmonary oedema • If pneumoconiosis is left out of the cause of death the decision still lies with the PMP. If pneumoconiosis is included and the PMP disagree then the PM report may be used to fuel a legal dispute by the relatives. • Simple pneumoconiosis is not per se considered to cause death but may be considered a factor in the death if associated with widespread chronic respiratory disease or cor pulmonale. • CWP is not related to carcinoma (may be inversely related due to smoking restrictions)

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Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003

SILICOSIS • a less massive, more solid form of PMF can occurr • all the other complications of cwp are seen (fibrous distortion, emphysema, TB, cor pulmonale) • peripheral plasma cells are characteristic ASBESTOSIS • the PMP decide on compensation for asbestosis or its neoplastic complications • pleural plaques denote asbestos exposure but per se are of no significance • asbestosis is worse in the lower zones and associated with numerous asbestos bodies. It is the only form of pneumoconiosis associated with cancer. • all cases diagnosed are referred to the MRC Pneumoconiosis Unit at Llandough Hosp., Cardiff • histological difficulty in distinguishing carcinoma from mesothlioma in a patient with an industrial history of asbestos exposure does not matter as far as compensation is concerned.

Ch.7: Transportation Deaths • Take samples for alcohol if death occurred within 24hr of the accident • Distinguish primary from secondary injuries by their location, appearance, presence of paint etc • Try to decide if injuries are ante or PM • Consider carbon monoxide poisoning of drivers and pilots • Try to confirm the pattern of injury wrt the position of the occupant e.g. steering wheel injuries • Preserve any paint-flakes, gravel, rust, grease etc for identification • It is not sufficient to state cause of death - try to interpret the circumstance of the accident.

Ch.8: Head Injuries • A blunt instrument may cause a clear-cut laceration but with some bruising of the edges • A ‘black eye’ may be due to: • a blow to the orbit bruising lids and cheek • blood tracking under scalp (scalp injury from forehead to vertex - victim upright for hrs) • base of skull fracture in anterior fossa - blood tracks via broken orbital plates • Skull Fracture • coup (circular depression with radiating fissures) • contre-coup (e.g. orbital plate [with black eye] after blow to back of head) • motor-cyclist’s fracture • ring fracture arounnd the foramen magnum from a blow to the vertex or landing on feet • Brain Injury • determine mechanism of injury and distinguish injury from primary diease causing it • ‘pea-in-drum’ vs. ‘shear-strain’ & rotary model of traumatic injury • coup & contre-coup contusion with secondary cerebral and subaracnoid haemorrhage • Secondary changes: flattening of surface, herniations, mid-brain haemorrhages, I.C.H. • I.C.H. • Extradural: arterial, lucid interval • Subdural: bridging veins, longer lucid, extremes of age, chronic incidental encaps. • SAH: A pure SAH without other forms of meningeal h’ge, brain damage or fractures skull is highly unlikely to be due to injury (except CV-1). Rupture of a berry may coincide with some incident e.g. a fight or effort during employment. The ‘CV-1’ lesion = dmage to the 1st cervical vertebra with bleed from the vertebral artery à pure SAH. Thus examine upper neck tissues for deep bruising. • Intracerebral: Solitary large lesions in a natural site is unlikely to be due to injury. • Complications of Head Injuries: • meningitis may occur in a closed injury (h’togenous spread to a nidus of damaged tissue) • if epilepsy develops for the first time after young adulthood its post-traumatic association is strengthened. A depressed fracture or adhesions between the membranes and inside of the skull may be found at PM. • Spinal Injuries: hyperflexion, hyperextension and compression types.

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Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003

Ch.9: Poisoning • Blood, e.g. for alcohol: as soon as the primary PM incision is made in the neck, reflect the sternomastoid and expose the internal jugular vein. Hold a tube pressed across the skin margin with its opened end just below the level of the vein. Cut vein with a clean knife. Lift head / repeat other side if more is needed. Transfer blood to a clean tube held by an assisstant. Alternatively use cut ends of axillary / iliac veins by lifting arm / leg while tube is in position (clean out cavities first. Avaoid heart blood (? possible diffusion of small molecules across diaphragm). • Stomach contents. Clean the serosal surface. Poise over cutting board with a wide receptacle underneath. Cut mid part of greater curve. Retain any granules / tablet fragments. • Urine: Clean and incise dome then immerse a tube or use a syringe. • Small intestine contents: send intact bowel with its contents and a string ligature at either end. • Liver: 500g of liver may allow an estemate of total liver content of drug by lab. • Other: bile, vitreous, CSF. • Record ‘continuity of evidence’ (whome sample given to at each stage) • Common drugs: • paracetamol • barbiturates: cause nearly all cases of ‘dead’ people who wake up in the mortuary. • salicylates: a few drops of 10% ferric chloride added to bladder urine / mucosa gives a deep Prussian blue. Sensitive but not specific. • tranquilizers, antidepressants and hypnotics. • Paraquat (Weedol / Gammoxone): proliferative lung fibrosis, centrilobular liver necrosis, renal tubular damage • Cyanide: Dark pink hypostasis, bright pink internal blood. Beware fumes from stomach! • Alcohol: The presence of copious fluid gastric contents in the airways can more firmly be used as the immediate cause of death. More chronic drinkers die from trauma rather than liver faiure. Back calculations from blood levels are unreliable due to multifactoriality.

Ch.10: Deaths from Extremes of Temperature: Hypothermia & Burns HYPOTHERMIA • dusky pink patches around large joints and on the extensor surfaces • small gastric erosions (parasympathetic) • fat necrosis in and around pancreas BURNS AND SCALDS • 9% each for head, arm, front of leg, back of leg; 18% for front or back of trunk.(die if >30%, >60yr) • Moist Burns (Scalds): • Usually children / women due to accidental spillage • Tissue damage without singing / hair damage. Blisters • Sharp demarcation at clothing edges • Dry Burns • Before or after death?: • A vital reaction is proof of antemortem burning (PM blisters do not have a surrounding red zone). • If soot and carbon are found in the trachea or distally then respiration must have occured during the fire. • If the tissues contain >10% saturation of CO then the victim must have been alive but if there is no CO this does not mean that he must have been dead. • >30% CO causes death / unconciousness esp. in old people or children. • Injuries on the body • Heat to the skull àexpansion of the contents à brittle cracks (d/dg fracture) • Blood boils to form a foamy brown extradural haematoma (d/dg e.d.h’ge) • Cracks in the scalp due to contracture of the skin (d/dg lacerations) • Identity of the victim: e.g. dental • Autopsy: Internal tissues usually better preserved, can take blood from them etc. • Suicide, Accident or Homicide?: stab wounds, bullets and strangulation • Corrosive Chemicals: acids à dark + leathery; alkali à moist + sloughy

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Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003

Ch.11: Immersion & Drowning • Immersion: rapid reflex cardiac arrest or death from other causes prior to entry. • Drowning: • Freshwater is hypotonic and flows rapidly through the pulmonary capillaries overloading the heart and causing lysis of rbcs with K+ release. Death is rapid. • Saltwater is hypertonic (3%), there is no mass fluid transfer and death is slower with a strong asphyxial component. • PM Signs of Immersion in Water: maceration, cutis anserina, pink lividity, foreign material in the mouth stomach and airways (not proof of drowning), cadaveric spasm (sudden immersion death). There are never petichial haemorrhages in the eyelids and lips. • PM Signs of Drowning: Froth in mouth / nostrils, large amount of water in stomach / airways (not proof and ‘dry lung drowning’ is common), overdistension of the lungs. • Tests for drowning: Chemical tests on the blood of the left cf right side of the heart are unreliable. The diatom test may be helpful but has technical difficulties. Litres of water from the scene must be examined. Diatoms are silicatious and can be concentrated by acid digestion of tissue samples (sternal bone marrow, brain, liver, kidney and lung). • Dating: Usual criteria are distorted. Living fleas upto 24hr, adipocere at least a few weeks • Injuries: Antemortem and PM may be difficult to distinguish due to the action of water, crabs etc • No opinion about the cause of death should be given on the PM appearances without a full appreciation of the surrounding circumstances.

Ch.12: Injury from Physical Agents: Electricity & Lightning • Voltage is important for causing local lesions, current for causing death. 20mA may kill if prolonged for more than about a minute, 50mA is rapidly fatal within a few seconds. Death is rare with less than 100V although even 12V can be lethal if there is sufficient current for a sufficient legth of time. Dry skin is 1MΩ, wet skin is 100Ω. The 50Hz of AC mains is approx. the same frequency as VF. Very high voltages may be safer as they convulse the person away from the source. When a hand grips a live conductor there is the danger of a ‘hold-on’ effect. • Types of Electrical Lesion • Firm contact raises an inconspicuous blister with little/no inflammatory reation • Poor contact raises a yellow nodule of fused keratin with a blanched areaola due to capillary contraction. This is due to sparking. • Cause of Death • VF arrest due to passage of current across chest • Respiratory failure due to diaphragmatic + intercostal paralysis with an asphyxial picture of congesion and petichiae of the pleura and pericardium. Central respiratory failure may be due to passage of current through the head. • Delayed death due to the complications of extensive burns. • Deaths are usually accidental followed by suicidal. Murder is rare. • Lightning: 20MV, 100,000sA. <50% mortality. Extensive burning is unusal, there may be marked oedema at the strike site and ferning fades within a few hours. Clothes may be ripped off due to explosive expansion of trapped air and metal objects melted or magnetised.

Ch.13: Deaths & Injuries from Firearms and Explosives • ‘A shot woman is a murdered woman until proved otherwise’. • Range of wound is important - if beyond arms reach of the trigger, an accident is then confined to some other person’s actions. • Site is a clue - suicides like the front of the chest, the temple, the mouth and less often the neck. It is very rare for the abdomen or the eye to be used and obviously inaccessible site should arouse suspicion of accident or crime. • Beware the use of exploding amunition! Many hollow-tipped bullet’s detonators fail to explode on impact and can be a danger to the doctor removing them.

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