Documente Academic
Documente Profesional
Documente Cultură
com) 1999-2003 1
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
• 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
Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003 2
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
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
Copyright © Dr P. J. Tadrous (www.bialith.com) 1999-2003 3
• 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)
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’
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.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.