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Pathophysiology of asphyxia & drowning

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Pathophysiology of asphyxia & drowning

  1. 1. Patho-physiology of Asphyxia
  2. 2. Asphyxia-Definition • Asphyxia: A Greek word literal meaning “pulse-less-ness or absence of pulsation”. • Condition caused by interference with respiration, or due to lack of O2 in respired air, due to which the organs & tissues are deprived of O2 (together with failure to eliminate CO2) causing unconsciousness or death. • “the physiological and chemical state in a living organism in which acute lack of oxygen available for cell metabolism is associated with inability to eliminate excess of carbon dioxide” (Adelson) • “(State) condition of the body in which the supply of 02 to the blood and tissues has been reduced appreciably below minimum critical level for maintenance of vital functions of the body by any mechanical interference with respiration”
  3. 3. Normal levels of oxygen in the arterial blood (pO2) with a 95% saturation of haemoglobin range from: • 90 to 100 mmHg(12-13.5 KPa) at age of 30 years • 65–80 mmHg ( about 10KPa) >60 years • Hypoxia: <60 mmHg (< 8 Kpa) even though the haemoglobin is 90% saturated; • Severe hypoxia: 40 mmHg (8-5Kpa) • Death: <20 mmHg (5-3Kpa)
  4. 4. Gordon’s Classification (1944) • • ANOXIA- lack of oxygen • Anoxic Anoxia: 02 from atmosphere cannot get entry into blood. e.g. Hanging, Strangulation, Smothering, Choking, traumatic asphyxia etc. • • Anaemic Anoxia: i.e. inability of blood to carry sufficient oxygen due to low haemoglobin contents • • Stagnant Anoxia: i.e. where the circulation of blood is impaired so that there is lack of oxygenated blood transport to the tissues • • Histotoxic Anoxia: O2 although freely available in the bloodstream—cannot be utilized by the tissues
  5. 5. Histotoxic anoxia(sub-division) • Extracellular, i.e. tissue oxygen enzyme system is poisoned Eg: cyanide poisoning, in which the cytochrome-oxidase system is interfered with. The effects of most of hypnotic and anaesthetic drugs may also be included in this because they depress cellular enzyme activity. Aluminium phosphide poisoning. • Pericellular- oxygen cannot gain access to the cell because of the decrease in the cell membrane permeability that may be seen in lipid soluble anaesthetic agents like halogenated hydrocarbons, e.g. chloroform, halothane, etc. • Substrate: i.e. there is inadequate food for efficient metabolism by the cell • Metabolite histotoxic hypoxia- the end products of cellular respiration cannot be removed thereby preventing further metabolism as in uraemia or CO2 poisoning
  6. 6. Stages of Asphyxia – 3 stages • (1) Stage of forced respiration: - It is due to stimulation of the respiratory center. - Clinical picture: DYSPNEA • (2) Stage of convulsions: - It is due to cerebral irritation. - Clinical picture: CONVULSIONS, CYANOSIS, HYPERTENSION, LOSS OF CONSCIOUSNESS, CONSTRICTED PUPILS. • (3) Stage of paralysis: - Clinical picture: LOSS OF CONSCIOUSNESS, FLACCID MUSCLES & LOST REFLEXES, DEEP CYANOSIS, DILATED PUPILS, IRREGULAR BREATHING (Cheyne-Stokes respiration). **Death occurs in about 3-5 minutes..
  7. 7. Rule of thumb • The breathing stops within 20 seconds of cardiac arrest and Heart stops within 20 minutes of stoppage of Breathing ‘Anoxia begets anoxia’
  8. 8. Vicious cycle of asphyxia reduction in O2 tension Capillary dilatation Capillary stasis Capillary engorgement Stasis of blood in organs Diminished venous return to heart Reduced pulmonary flow Deficient oxygenation in lungs Asphyxia
  9. 9. Asphyxia Triad 7/25/2014 9 Congestion & Edema Cyanosis Petechial Hemorrhage
  10. 10. Asphyxial Triad 1. PETECHIAL HAEMORRHAGES: Due to increase pressure on thin walled peripheral venules and capillaries..no role of Hypoxia, also seen in coughing,sneezing , SIDS, H’gic diathesis….disappears with PM interval..can apppear & enlarge PM phenomenon, abnormal postures, seen in normal and ‘congestive’ deaths, not all punctate lesions in pleura are petechiae, unreliable however in eyelids, conjuctiva n sclera needs explanation unless body was head/face down
  11. 11. 1. 2. CYANOSIS: Due to reduced oxygen supply to the tissue, more than 5gm% should be in form of reduced Hb. Greek word meaning ‘dark blue’…not apparent in anemia….it can be overshadowed by Hypostasis 3. CONGESTION AND EDEMA: Due to reduced venous return, Edema is due to rapid transduation thru capillaries & venule walls
  12. 12. Asphyxia CLINICAL EFFECTS OF ASPHYXIA Sphincter relaxation Voiding of urine, stools, semen Decreased oxygen tension and reduced Hb Cyanosis Capillary endothelium damage Increased capillary permeability Pulmonary edema Unconsciousne ss Loss of muscle power Capillary stasis and engorgement Increased intracapillary pressure Capillary rupture Tardieu’s spots
  13. 13. Other signs 4. PULMONARY OEDEMA: Attempts to inspire against closed airway generates a negative pressure which leads to increased capillary permeability as the alveoli and capillaries are damaged. 5. FLUIDITY OF BLOOD: Increased permeability and degeneration of cell membrane leads to release of plasminogen activator, which increase fibrinolytic activity and prevents clotting of blood. 6. BLEEDING FROM EAR & NOSE 7. DILATATION OF RIGHT CHAMBERS OF HEART
  14. 14. Ischemic Brain Damage • Brain receives 20% of total Oxygen though it is only 1.4% body wt, has autoregulatory vascular control mechanism • Neurons are highly vulnerable to hypoxia because of presence of acidic excitatory neurotransmitters- EXCITOTOXINS • Neurons die in 3 to 7 minutes in anoxia • Factors that determine Brain damage are -severity of Hypoxic episode, age of Pt., other CNS diseases, body Temp. • In all different forms of Anoxia the end result to brain is ischemic brain damage which may have following patterns: Hypoxic-ischemic encephalopathy Cerebral infarction
  15. 15. Pulmonary edema • The cause of the pulmonary edema can either be due to anoxic injury to the central nervous system (neurogenic pulmonary edema) or from the large negative intrathoracic pressures seen when the victim struggles to breathe in against an occluded airway (obstructive pulmonary edema).
  16. 16. Post mortem findings: Classical Signs, Nonspecific signs & Specific signs • External: congestion, edema, petechiae (0.1-2 mm), echchymosis(> 2mm), cyanosis, deep PM staining, protrusion of tongue, bloody and frothy fluid from mouth and nose, Swelling of face, Prominence of eye balls, spontaneous defecation, urine & sperm excretion • Note: It is never justified to call one died due to asphyxia, only on general, non specific pathological features although present in most cases, they must be supplemented by specific signs.
  17. 17. Post mortem findings(contd..) • Internal: Tardieu spots, dark & fluidity of blood, vomitting could be caused by medullary suboxia, congestion of organs, middle ear bleed. Emphysematous lungs, Pulmonary edema, with froth in trachea and bronchi, Bulky, crepitant and over-distended lungs, Right ventricular dilatation • If Heart stops before Respiration the asphyxial signs will be less.
  18. 18. Types (causes) of Asphyxia 1. MECHANICAL eg: a) Smothering b)Hanging/Strangulation/throttling c) Choking d) Drowning e) Traumatic Asphyxia 2. PATHOLOGICAL 3. TOXIC 4. ENVIRONMENTAL 5. TRAUMATIC 6. POSTURAL 7. IATROGENIC 7/25/2014 18
  19. 19. Histology • Disruption of alveolar septa with Hemorrhage in alveoli and edema • Brick red discoloration of nerve cells in Cortex • Pallor & Vacuolar degeneration of Purkinje cells in the cerebellum • Vacuolar degeneration of liver cells • Chemical marker- Hypoxanthine in blood & vitreous
  20. 20. Violent asphyxial deaths • Here the process of respiration i.e, the exchange of air between the atmosphere & Lung beds is prevented by some violent mechanical means • Types: Hanging Strangulations Drowning Suffocations
  21. 21. • Hypoxic injury to Brain • Hypostatic Pneumonia • Mediastinal emphysema
  22. 22. Possible effects of pressure on neck: • Explanation for Death due to Partial Hanging • • Carotid sinus reflex leading to cardiac arrest • • Jugular veins compression leading to cyanosis and petechiae: (2Kg. Tension) • • Carotid artery compression (3-5 Kg. Tension) leading to unconsciousness • • Airway obstruction leading to hypoxia. (15 Kg. Tension) • • Occlusion of vertebral artery. (20Kg.Tension), leading to unconsciousness
  23. 23. Modified Y-shaped incision at neck showing base of ligature mark – brownish black in colour. Usually it is pale, white and glistening.
  24. 24. Carotid sinus Baroreceptors
  25. 25. Complete Partial
  26. 26. Typical Atypical
  27. 27. Oblique, upwards, backwards, above the level of thyroid cartilage
  28. 28. Oblique, upwards, backwards, at or above the level of thyroid cartilage
  29. 29. Inverted V shape mark
  30. 30. Dribbling of saliva
  31. 31. Protrusion of tongue
  32. 32. Transverse tears in intima of both carotid arteries in case of hanging. It is due to combination of RADIAL FORCE ( ligature material)& AXIAL TRACTION( weight of body due to suspension)
  33. 33. Carotid intimal tears
  34. 34. Fracture of left cornu of hyoid bone with inward displacement. They are common in victims of age above about 40 years as the cornu gets calcified after that age.
  35. 35. Fracture of left cornu of hyoid bone with outward displacement.
  36. 36. Ingredients of Hanging • Suspension (POS) • Ligature encircling the neck • Constricting force • Ligature mark – oblique, incomplete, located above thyroid cartilage • Fracture of hyoid bone • Intimal tears of carotid • Pallor – underneath, extravasations in surrounding structures • Dribbling of saliva • Signs of asphyxia
  37. 37. Sr. No. Trait Hanging Strangulation 1 Ligature mark Oblique, incomplete, high in the neck Transverse, complete, mid level or below thyroid cartilage 2 Base Pale, hard, parchment like Contused 3 Abrasion, contusion & Echymosis Less prominent More prominent 4 Hyoid fracture More common Less common 5 Thyroid cartilage Less common More common
  38. 38. Sr. No. Trait Hanging Strangulation 6 Carotid Intimal tear Not seen 7 Signs of asphyxia Less marked More marked 8 Dribbling of saliva Often Rare 9 Bleeding from nose, mouth & ears Rare Often 10 Involuntary discharge Occasional Frequent 11 Manner Suicidal Homicidal 12 Injuries on other body parts Rare Common
  39. 39. Two parallel & transverse ligature mark on front of neck in case of strangulation. Bleeding from nostrils also present.
  40. 40. Extensive bruising and abrasions in a case of throttling
  41. 41. Bodies retrieved/ recovered from water may have: a) Died from sudden natural disease before falling into the water. -- A person walking near water falls in due to IHD/ CAD. b) Died from sudden natural disease while already in the water. c) Died from injury before being thrown into the water. d) Died from injuries while in the water. e) Died from effects of immersion other than drowning. -- exhaustion, exposure to cold waters( Titanic) f) Died from drowning.
  42. 42. Phases of drowning: 1. Breath holds 2. Inhalation of water, coughing, vomiting and loss of consciousness 3. Convulsions, respiratory arrest then cardiac arrest • BROUARDEL’S EXPERIMENT • Stage of surprise(5-10 seconds) • First stage of respiratory failure(1 min) • Stage of deep respiration (1 min) • Second stage of respiratory arrest(1 min) • Stage of terminal gasp (30 seconds)
  43. 43. Types: TYPICAL DRWNING 1. Wet drowning: Water is inhaled into the lungs a-salt water b. fresh water ATYPICAL DROWNING 2. Dry drowning; Water enters URT but not lungs. 3.Secondary drowning(near drowning) Delayed death after resuscitation after living victim is taken out of waters. 4. Immersion syndrome- Hydrocution Vagal inhibition as result of : a) water striking epigastrium b) Cold water entering ear drums, nasal passage, larynx, pharynx
  44. 44. POST MORTEM FINDINGS: [A] FEATURES OF SUBMERSION: -- Wet clothes and body surface -- Soiling with mud, grass etc. -- Cutis Anserina ( ? Molecular death) -- Washerwoman’s skin appearance: Pale , white, wrinkled, softened.
  45. 45. Autopsy signs of drowning (seen in 35% of cases) 1. Froth in nose and mouth 2. Pulmonary edema 3. Overdistention of lungs 4. Dry drowning 5. Middle ear hemorrhage 6. Chemical tests (unreliable) 7. Non-specific changes of immersion
  46. 46. Appearance of froth in case of typical drowning
  47. 47. [B] FEATURES OF ANTE-MORTEM SUBMERSION: -- Cadaveric spasm with firmly grasped vegetable materials etc. -- Froth : White = Colour Fine = small bubbles Lathery = soft consistency Tenacious = Adherent / sticky Copious = abundant, constant -- Haemorrhage in middle ear.( water through Eustachian tube ) Trait Fresh water Sea water -- Lungs 1. Size & weight Ballooned but light Ballooned & Heavy 2. Colour Pale pink Purplish / bluish 3. Consistency Emphysematous Soft 4. After removal Do not collapse Collapse 5. On cut section Crepitus heard Crepitus absent Froth , No fluid Froth + Fluid
  48. 48. • Paltauf’s Hemorrhage • Emphysema Aquosum • Edema aquosum
  49. 49. Cutis Anserina
  50. 50. WASHERWOMAN’S SKIN APPEARENCE: Pale , white, wrinkled, softened skin of palm due to prolonged exposure to water.
  51. 51. Specific signs • SIGN OF KRUSHEVSKY: full of small bubbles white foam in respiratory tracts • SPOTS OF RASSKAZOV-LUKOMSKY: reddening and edema of mucous tunic of respiratory tracts, increasing and emphysema of lungs, pale, dim hemorrhages on their surface • SIGN OF МОRO: presence of water in a small intestine and abdominal cavity, • SIGN OF SVESHNIKOV: presence of liquid of drowning environment in the sinus of sphenoid • increasing of liver in size and presence of plankton in inner organs;
  52. 52. Emphysema aquosum
  53. 53. DIATOM TEST: What are diatoms? Unicellular algae with outer siliceous wall. How they enter blood circulation? Through ruptured alveolar wall, diatoms up to size 60 microns enter the pulmonary veins & then to left side of heart, with blood circulation they are transported to bone marrow, brain & other organs. Technique of demonstration: 5 gm of marrow is collected from sternum bone and is subjected to acid digestion with 5 times volume of nitric acid for 1-2 days. Sediment is examined under phase contrast or dark ground illumination microscope. Interpretation of results: Control samples of water from site treated with Iodine is compared for type of diatoms.
  54. 54. Different common varieties of Diatoms:
  55. 55. Thank you

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