POST MORTEM CHANGES.pptx

PM Changes by Harrison Mbohe MBChB Level 4 JKUAT

1. POST MORTEM CHANGES IN RIGOR MORTIS, LIVIDITY, AUTOLYSIS & PUTREFACTION AND THEIR FORENSIC SIGNIFICANCE

2. RIGOR MORTIS Postmortem stiffening of body muscles. Pathophysiology Cessation of aerobic metabolism  ↓ ATP & ↑ Lactic acid. ↓ ATP  ↓ integrity of muscle  influx of Ca 2+  irreversible binding of actin & myosin  formation of actomyosin complex  muscles become hard & rigid. Progress: Onset – within 2 hrs after death Fully formed after approximately 12 hrs postmortem. Dissipates after about 36 hrs after death – due to muscle autolysis. Initially notable in the small muscles around the eyes and mouth, the jaw. Generally follows cranio-caudal progression.

3. Forensic significance : Not readily apparent in decedents with low muscle mass (emaciated, infants & elderly). Little utility as a marker of the PMI on its own – many confounders modifying the speed, onset and duration, mainly temperature. Body site specific artifacts Contraction of the left ventricle post mortem  misconstrued as LVH. Rigor of dartos muscle  post mortem ejaculation of semen  misconstrued as sexual activity before death. Rigor in the erector pili muscles  pimpling or ‘goose-bumps’ appearance with elevation of the cutaneous hairs. Rigor of ciliary muscles  pupil inequality  misconstrued as anisocoria. Electrocution and state of exercise before death  rapid onset rigor mortis. The colder the environment the slower the process and vice versa. Conditions which mimic rigor mortis: heat and cold stiffening, gas stiffening & cadaveric spasms

4. Full rigor mortis 12 hours post-mortem.

5. Cadaveric rigidity – here seen in a body recovered from water, where vegetation is found tightly ‘gripped’ in the hand.

6. LIVOR MORTIS Reddish-blue staining of low-lying dependent regions of the body. Pathophysiology: Cessation of circulation  failure of arterial propulsion & venous return  gravity pulls stagnant blood to low dependent areas. Progress: Initial appearance of discolored patches within 1-3 hrs after death. Patches ↑ in size and spread all over the dependent areas in 4 to 6 hrs after death. Full development; 6-8 hrs after death. Shifting of post-mortem lividity - change in body position before full development of livor mortis will cause blood to settle in new dependent regions. Fixation of post mortem staining - After full development, shifting is not possible due to coagulation of blood in the dependent areas

7. Post-mortem hypostasis in a posterior distribution. Areas of pallor can be seen as a result of pressure of the body on a firm surface. Parts of the body not in direct contact with that surface are purple/ pink because of the ‘settling of blood under gravity’. This body has been lying on its back since death.

8. Post-mortem hypostasis in a death from hanging. The discoloration of the skin is in the legs and hands, due to the vertical posture after death.

9. Post-mortem hypostasis pattern on the front of a body found face down on a bed. The linear marks are formed by pressure from creases in a blanket. Pallor around the mouth and nose are caused by pressure against the bed

10. Forensic significance May be absent in the young, the old and the clinically anaemic or in those who have died from severe blood loss. May be also masked by dark skin colours, by jaundice or by some dermatological conditions. Haemorrhage behind the oesophagus at the level of the larynx  misconstrued with the trauma of strangulation. Internal organs affected by livor mortis may be misconstrued as disease e.g., myocardium (dark patch in the posterior wall of the left ventricle ) – MI. Meninges – SAH Lungs – pneumonia. Color & character of livor mortis may suggest a cause or mechanism of death Cherry pink – CO toxicity, hypothermia Dark blue – pink/red hue – cyanide toxicity. Bronze – infection by C. perfringens Brownish red - methemoglobinemia

11. Forensic significance The time taken for hypostasis to appear is so variable that it has no reliable role in determining the time of death. To avoid livor mortis associated artifacts, bodies should be stored and transported face up. The colour of hypostasis is variable and may extend from pink to dark pink to deep purple and, in some congestive hypoxic states, to blue . Identifying bruises in areas of lividity;- Incise the suspect area to see if the underlying blood is intravascular (hypostasis) or infiltrating the tissues outside the vessels (contusion). Apply pressure to identify if blanches – bruises don’t blanch.

12. AUTOLYSIS & PUTREFACTION AUTOLYSIS Aseptic breakdown of cells and tissues by liberated enzymes. Many changes are appreciated at a microscopic level. Accelerated by: Intoxications with bio membrane solvents, heat, high humidity, and pathologies such as infectious diseases, acute pancreatitis. Slowed by: Dry environment and large concentrations of enzyme inhibitors and inactivators e.g., mercury, and arsenic. On autopsy, the doughy appearance of the pancreas and lungs appear within hours of death. The aseptic autolysis of the still born fetus is known as maceration.

13. Maceration following intrauterine death. Note the widespread skin slippage and cord strangulation.

14. Putrefaction Septic component of decomposition. Results in liquefaction and gaseous formation of the soft tissues. Modifying factors including: Ambient temperatures, bacteremia, exposed body cavities, prone body position, burial, and submersion in water. First sign include; green discoloration of abdomen in the RLQ.

15. Characterized by; Skin discoloration – green, deep red and black. Marbling; bacterial proliferation within superficial veins -  venous distribution in the skin Bloating of the face, abdomen, breasts and genitals – due to gaseous distension. Leakage of purge fluid due to acc of gases  ↑ internal pressure  protrusion of the eyes & tongue and forces blood-stained fluid up from the lungs which often ‘leaks out’ of the mouth and nose. Skin slippage and epidermal blistering – peeling of the epidermis in a glove and stocking fashion of the hands & feet, respectively; hair and nails detach.

16. ‘marbling’ of the skin

17. ‘Bloating’ of soft tissues, distortion of facial features and ‘purge fluid’ emanating from the mouth and nose.

18. Forensic significance Distorted bloating of the neck and face makes visual identification difficult or impossible. Skin slippage causes shedding of the outer layers of the fingers and toes, making identification by fingerprints more difficult. Purge fluid may be mistaken for antemortem hemorrhage. Breakdown of the pancreas mimics hemorrhagic pancreatitis. Distension from gas and softening of the gastrointestinal tract may cause an artefactual rupture. The early changes of decomposition may be confused with the signs of violence or trauma.

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