Pathogenesis and Medicolegal aspect of shock


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shock is one of the main cause of death very common encountered in day to day practice,in this presentation we look at how it happen,what are the causes and how we diagnose it in brief and its forensic importance

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Pathogenesis and Medicolegal aspect of shock

  1. 1.  Shock is any condition in which the circulatory system is unable to provide adequate circulation to the vital body organs such as the brain, heart and lungs. As a result of a decrease in the blood pressure.  Shock is usually accompanied by renal failure, as a normal compensatory mechanism, because the blood flow to the kidney is decreased to keep enough blood for the vital organs.
  2. 2.  Shock is classified according to the causes to four classes:  Hypovolemic shock  Distributive shock  Cardiogenic shock  Neurogenic shock
  3. 3.  1.Hypovolemic shock is caused by low blood volume.  Normal blood volume is 5 L and by losing 1- 2 L it can lead to shock.  The Decrease in blood volume is caused by:  External blood loss: ex. Hemorrhage  Internal blood loss: ex. Ruptured spleen caused by blunt trauma.  Severe dehydration as a result of:  Vomiting  Diarrhea  This is a typical condition in cholera.  Burns
  4. 4.  2. Distributive shock is caused by excess vasodilatation (ex. Anaphylactic shock and septicaemia)  Vasodilatation Arteriole resistance increase blood exchange from the vessels to the peripheral tissues decrease blood return to the heart BP shock.  Anaphylaxis, drug, toxin reactions  Trauma: crush injuries, major fractures, major burns.  Infection/sepsis: G(-/+ ) septicemia, pneumonia, peritonitis, meningitis, cholangitis, pyelonephritis, necrotic tissue, pancreatitis, wet gangrene, toxic shock syndrome, etc.
  5. 5.  3.Cardiogenic shock ( heart does not pump enough blood) is caused by:  A) Myocardial infarction leads to weak cardiac As a result Muscle contraction Ischemia of  B) Arrhythmia ( such as ventricular fibrillation, which will stop the heart pump and that will decrease BP)  Note: Supraventricular (Atria) fibrillation will not cause shock because 75% of the blood transfer from the atrium to the ventricles by passive transport.
  6. 6.  C) Valve problems, ex. Valvular stenosis which is narrowing of the valves, or leakage of blood through the valves ( Regurgitation).  D) Problems in the A-V shunt.  4.Neurogenic shock  Mechanism: Loss of autonomic innervation of the cardiovascular system (arterioles, venules, small veins, including the heart)  Causes:  Spinal cord injury  Regional anesthesia  Drugs  Neurological disorders
  7. 7. PATHOGENESIS:- HYPOVOLAEMIC SHOCK Effective circulating blood volume Haemorrhage Trauma Venous return Surgery to heart Burns Dehydration SEPTIC (TOXAEMIC) SHOCK Gram-ve septicaemia Gram+ve septicaemia
  8. 8. CARDIOGENIC SHOCK Cardiac output Deficiency of emptying Deficiency of filling Blood flow Outflow obstruction Supply of oxygen OTHER TYPES Traumatic shock Anoxia Neurogenic shock Hypoadrenal shock Inflammatory mediators SHOCK
  9. 9. Common mediators of septic shock include TNF-α, IL-1, NO, and Ceramide. All of these cytokines released during sepsis cause extreme diffuse vasodilation and vascular leakage, leading to distributive shock. Reduced SVR is a hallmark of septic shock.
  10. 10. Hypoxic Cell injury Activation of innate immunity Stimulation of macrophages Release of inflammatory mediators TNF-α IL-1 Others Synthesis of Vasodilatation Other cytokines Nitric oxide (IL-6, 12, 8, PAF) Generation of Hypotension Free radicals Free radicals C3a, C5a Figure: Response of inflammatory mediators in shock.
  11. 11.  Kidneys  Shock causes “pre-renal” acute renal failure. Ischemia of tubule epithelium leads to vasoconstriction, reduced GFR, oliguria, and azotemia  Ischemia leads to Acute Tubular Necrosis (ATN)  Brain  Altered mental status occurs early in shock, due both to hypoxemia and metabolic problems  GI tract  The GI tract is at very high risk of infarction. Shock causes infarction of the GI epithelium
  12. 12.  Liver  Centrilobular necrosis is common. There is diminished reticuloendothelial clearance  Blood -- DIC  WBC count may go up or down.  Platelets go way down as they are all used up in DIC.  Diffuse fibrin thrombosis consumes feedback inhibitors, leading to more and more clotting
  13. 13.  Shock leads to multi-organ dysfunction syndrome (MODS).  The lungs are usually the first organ to fail, followed by kidneys, liver, GI tract, and then brain.  Heart  Grossly, subendocardial hemorrhages are common.  Microscopically, contraction bands are seen in myocardial cells.  Fatty change – 18 to 24 hrs well marked in 3 to 4 days
  14. 14.  Lung  Shock causes release of inflammatory mediators such as TNF-α. This injures endothelial cells.  Endothelial injury allows leakage of proteinaceous fluid and neutrophils into the interstitium.  interstitial edema and inflammation common in shock.  Edema is well discernible after 2 to 3 days  Since it’s interstitial, not alveolar, the septae between alveoli are greatly widened.  Lungs become heavy, stiff, and hemorrhagic.
  15. 15.  Brain  Watershed infarcts are a common consequence of shock. These are long, wedge-shaped infarcts at the very distal tips of a major arterial supply.  Laminar necrosis is another common consequence of shock.  GI tract  Shock often causes mucosal hemorrhage and necrosis  Grossly, the GI tract may appear swollen and bloody.  Adrenal  The may be evidence of focal lipid depletion in the cortical area within 1 to2 days
  16. 16.  Liver  Fatty change become evident within 18 to 24 hrs  Shock generally causes centrilobular necrosis, because the hepatocytes closest to the central vein are the furthest from the blood supply.  Kidneys  The most susceptible kidney cells are those in the proximal tubules and thick ascending Loop of Henle.  Microscopically, you will see acute tubular necrosis (ATN). There will be dilation of proximal tubules due to flattening of the epithelium. Brownish casts may be seen
  17. 17.  In a person with haemorrhagic diathesis or haemophilia, minor injury produce death from hge.  A trivial bruise causes loss of 20-30ml of blood loss. So an extensive bruise without any other injury might also cause dead .  Examination of crime scene is important to calculate the amount of blood loss.  Men withstand hge better than women.  Sudden rise of BP in neurogenic shock can precipitate serious complications like –  (a) Intracerebral hge from rupture of arteriosclerotic cerebral vessels or of berry aneurysm.
  18. 18.  (b) Rupture of a dissecting aneurysm of aorta.  Under such conditions even when the deceased received minor trauma before death, the essential cause of death will be underlying disease process.  Minor stimuli or injury over receptic spots may cause sudden death from neurogenic shock.  In persons of neurotic or emotional temperament, in deeply intoxicated, severely ill or feeble old and young children, death from primary shock occurs readily.
  19. 19.  Shock is a complex, dynamic disorder of tissue and cellular hypoperfusion, produced by multiple interacting mechanisms that may lead to MODS & death. Successful treatment of patients with shock requires prompt recognition of the shock state and a thorough understanding of the pathophysiology of various types of shock
  20. 20.  In case of any sudden death meticulous history taken to rule out any precipitating factor of shock is a must.  There may not be any evidence of injury in some cases of death from violence.  E.g sudden death due to vagal inhibition  In such case after full and meticulously done autopsy, even absence of violence or morbid cause to account for sudden death of the subject who was ordinarily healthy previous to infliction of violence there might not to be any hesitation to ascribe the death to be due to functional effect of the injuries.
  21. 21.  Autopsy finding in case of death due to neurogenic shock are mainly inferential and the diagnosis is arrived at from history of sudden death following blow or injury over the area and negative finding. E.g absence of fatal injuries, poisoning or natural disease etc  So careful history taking is a must besides other investigations in establishing the cause of death.