Forensic Medicine & Toxicology.
By:
Dr. Amina Afzal Rao
ASPHYXIA
ASPHYXIA
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.
TYPES OF ASPHYXIA
1- MECHANICAL
2- PATHOLOGICAL
3- TOXIC
OBSTRUCTION
DISEASE
PRESENCE OF
POISONOUS
GASES LIKE CARBON
MONOXIDE
4- ENVIRONMENTAL VITIATED ATMOSPHERE
OF DEEP WELLS
5- IATOROGENIC
IN ANAESTHESIA
SURGERY
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.
-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.
-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.
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
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.
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--
BIOCHEMISTRY OF FATAL ASPHYXIA
O2 AND CO2 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.
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.
-RUPTURE OF SMALL CAPILLARIES--- PERMEABILITY
PRODUCES PETECHIAL HAEMORRHAGES.
GENERAL PATHOLOGICAL CHANGES OR
ASPHYXIA:
-GENERALIZED CYANOSIS
-VASCULAR CONGESTION
- OEDEMA OF TISSUES /VISCERA
-FLUIDITY OF BLOOD