1. Forensic Medicine & Toxicology. By: Dr. Amina Afzal Rao ASPHYXIA

2. IT IS DEFINED AS INTERFERENCE WITH THE PROCESS OF OXYGENATION IN THE LUNGS. THE ESSENTIAL FEATURE OF ASPHYXIA IS STRUGGLE TO BREATHE AGAINST SOME KIND OF INTEFERENCE WITH RESPIRATION.

3. TYPES OF ASPHYXIA 1- MECHANICAL OBSTRUCTION 2- PATHOLOGICAL DISEASE 3- TOXIC PRESENCE OF POISONOUS GASES LIKE CARBON MONOXIDE 4- ENVIRONMENTAL VITIATED ATMOSPHERE OF DEEP WELLS 5- IATOROGENIC IN ANAESTHESIA SURGERY

4. COMPRESSION OF NECK CAUSES -OBSTRUCTION TO BLOOD FLOW -OBSTRUCTION TO BREATHING -OBSTRUCTION TO VENOUS BLOOD RETURN FROM HEAD CAUSES CONGESTION AND HAEMORRHAGES ABOVE THE LEVEL OF CONSTRICTION. -OBSTRUCTION TO ARTERIAL BLOOD FLOW CAUSES.BLOCKAGE OF CAROTID ARTERIES -------- ------ANOXIA OF BRAIN AND UNCONSCIOUSNESS.

5. -PARTIAL BLOOD FLOW CONTINUES THROUGH VERTEBRAL VESSELS. - PRESSURE ON THE CAROTID SINUS AND VAGUS NERVE MAY PRECIPITATE REFLEX CARDIAL ARREST. -OBSTRUCTION TO THE WINDPIPE CAUSES GENERALIZED OXYGEN DEFICIENCY.

6. -LARYNX IS LIFTED UP SO THAT THE TONGUE BLOCKS THE BACK OF THE THROAT. -PRESSURE ON THE LARYNX------ HYOID BONE THYROID CARTILAGE MAY CAUSE THEIR FRACTURES AND INJURIES TO OTHER SOFT TISSUES. SITES OF FRACTURES -------??? TWO MECHANISMS----DIRECT LATERAL COMPRESSION----AND INDIRECT THROUGH PRESSURE ON THE THYROHYOID LIGAMENT.

7. EFFECTS OF PRESSURE ON NECK -CAROTID SINUS PRESSURE –VAGAL STIMULATION—CARDIAL ARREST. -CAROTID ARTERY BLOCKAGE– UNCONSCIOUSNESS -JUGULAR VEIN BLOCKAGE-----CONGESTION AND HAEMORRHAGES -AIRWAY BLOCKAGE—OXYGEN LACK

8. PHYSIOLOGY OF ASPHYXIA STUDIED BY SWANN AND BRUCER—ON DOGS. THREE PHASES OF EXTREMELY SHORT DURATION UNCONSCIOUSNESS OCCURS IN ONE MINUTE FOLLOWED BY DEATH IN ABOUT 3-4 MINUTES.

9. PHASE I: STIMULATION OF RESPIRATION CYANOSIS PHASE II: STRUGGLE TO BREATHE DEEP CYANOSIS, ENGORGEMENT OF NECK VEINS– PETECHIAL HAEMORRAGES CONFUSION— UN CONSCIOUSNESS. PHASE III: UNCONSCIOUSNESS– COMA IRREGULAR BREATHING ---SLOW RESPIRATION ---FAILURE--- HEART CONTINUES TO BEAT –PUPILS PILATED--

10. BIOCHEMISTRY OF FATAL ASPHYXIA O 2 AND CO 2 IN BLOOD -LOWERING OF BLOOD PH-----ACIDIC BSL---, -EXCHANGE OF SODIUM AND POTTASIUMIONS ACROSS THE CELL MEMBRANE – DEATH OF CELLS MAY OCCUR DUE TO DEGENERATION.

11. PATHOLOGY OF FATAL ASPHYXIA -CAPILLOVENOUS ENGORGEMENT WITH RISE IN LEVEL OF CO2 INCIRCULATING BLOOD CAUSES -GENERALIZED CONGESTION -CYANOSIS ANOXIA INCREASE PERMEABILITY OF CAPILLARY WALL ---FLUID OUT INTO TISSUE SPACES—AND TRANSUPATION OF PLASMA INTO TISSUE SPACES CAUSES OEDEMA.

12. -RUPTURE OF SMALL CAPILLARIES--- PERMEABILITY PRODUCES PETECHIAL HAEMORRHAGES. GENERAL PATHOLOGICAL CHANGES OR ASPHYXIA : -GENERALIZED CYANOSIS -VASCULAR CONGESTION - OEDEMA OF TISSUES /VISCERA -FLUIDITY OF BLOOD