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6. embolism; hemodynamic disordrs

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6. embolism; hemodynamic disordrs

  1. 1. Hemodynamic Disorders Edema Hyperemia and Congestion Hemorrhage Hemostasis and Thrombosis Embolism Infarction Shock Dr. Krishna Tadepalli, MD, www.mletips.com
  2. 2. Embolism Embolism  Can be solid ((thrombus), Liquid (Amniotic fluid) or Gas  Can be solid thrombus), Liquid (Amniotic fluid) or Gas (Air, Nitrogen) carried by blood flow from the site of (Air, Nitrogen) carried by blood flow from the site of origin origin  Most commonly  detached thrombus = also called  Most commonly  detached thrombus = also called thrombo – embolism thrombo – embolism  Rarely  Fat, Air/ Nitrogen, Cholesterol emboli, Tumor  Rarely  Fat, Air/ Nitrogen, Cholesterol emboli, Tumor emboli, Foreign bodies emboli, Foreign bodies  Consequence  vascular obstruction  Infarction  Consequence  vascular obstruction  Infarction  Types  systemic (arterial), Pulmonary  Types  systemic (arterial), Pulmonary Dr. Krishna Tadepalli, MD, www.mletips.com
  3. 3. Emboli - Types Systemic Pulmonary Systemic Pulmonary  Arterial ((exception  Arterial exception  Paradoxical ))  Paradoxical  Arise in heart  Arise in heart  Cause infarctions  Cause infarctions lower extremities – lower extremities – 75%, Brain (15%), 75%, Brain (15%), Kidney, spleen) Kidney, spleen) • Venous • Venous • DVT • DVT • Emboli cause • Emboli cause Pulmonary embolism Pulmonary embolism ((silent in 50% of pts.). silent in 50% of pts.). If 60% of pulmonary If 60% of pulmonary circulation is blocked circulation is blocked  sudden death due to  sudden death due to acute cor -pulmonale acute cor -pulmonale (Rt. Heart Failure) (Rt. Heart Failure) Dr. Krishna Tadepalli, MD, www.mletips.com
  4. 4. Embolism Pulmonary embolism Dr. Krishna Tadepalli, MD, www.mletips.com
  5. 5.  Pulmonary embolism  Pulmonary embolism Dr. Krishna Tadepalli, MD, www.mletips.com
  6. 6. Fat embolism Fat embolism  Causes Most common (90%) with fractures of long  Causes Most common (90%) with fractures of long bones, less commonly following soft tissue trauma, Burns bones, less commonly following soft tissue trauma, Burns  When ?? 3-5 days after the injury  When  3-5 days after the injury  Clinical  Heart =Tachycardia  Clinical  Heart =Tachycardia  Lungs Tachypnea,  Lungs Tachypnea,  Blood  Petechiae, Anemia  Blood  Petechiae, Anemia  Mechanism  Mechanical ((obstruction)  Mechanism  Mechanical obstruction)  Biochemical Neutral fats cause platelet & RBC aggregation  Biochemical Neutral fats cause platelet & RBC aggregation and destruction and destruction  Free fatty acids endothelial injury  Free fatty acids endothelial injury  Diagnosis  Frozen sections stained with fat stains ((oil  Diagnosis  Frozen sections stained with fat stains oil red –O, Sudan IV) red –O, Sudan IV)  Hematological findings (anemia, Petechiae on  Hematological findings (anemia, Petechiae on nondependent parts) are very useful nondependent parts) are very useful Dr. Krishna Tadepalli, MD, www.mletips.com
  7. 7. Fat Embolus Special stain ALVEOLI Dr. Krishna Tadepalli, MD, www.mletips.com
  8. 8. Air embolism Air embolism  Causes obstetric (pregnancy), chest wall injuries,  Causes obstetric (pregnancy), chest wall injuries, sports( scuba diving), occupational (caisson’s) sports( scuba diving), occupational (caisson’s)  Clinical  acute  in scuba divers, obstetric, injuries  Clinical  acute  in scuba divers, obstetric, injuries  Chronic  caisson’s  Chronic  caisson’s  Bends  joint pains, chokes  pulmonary  Bends  joint pains, chokes  pulmonary  Mechanism  physical ((circulatory gap), Nitrogen in  Mechanism  physical circulatory gap), Nitrogen in scuba divers, caisson’s disease scuba divers, caisson’s disease  Lethal dose  100 cc  Lethal dose  100 cc  Complications  ischemic necrosis of heads of long  Complications  ischemic necrosis of heads of long bones bones  Treatment  slow decompression in compression  Treatment  slow decompression in compression chambers chambers Dr. Krishna Tadepalli, MD, www.mletips.com
  9. 9. Amniotic Fluid embolism Amniotic Fluid embolism  Causes leak of Amniotic fluid into maternal circulation  Causes leak of Amniotic fluid into maternal circulation  Mechanism  thrombogenic  DIC, Mechanical  Mechanism  thrombogenic  DIC, Mechanical obstruction obstruction  Clinical  uncommon but most important cause of  Clinical  uncommon but most important cause of maternal mortality ((30% deaths) maternal mortality 30% deaths)  Pulmonary  Dyspnea, Tachypnea, later pulmonary  Pulmonary  Dyspnea, Tachypnea, later pulmonary edema and ARDS edema and ARDS  CVS Hypotensive shock  CVS Hypotensive shock  CNS Seizures, coma  CNS Seizures, coma  diagnosis  pulmonary emboli with Lanugo hair, fetal  diagnosis  pulmonary emboli with Lanugo hair, fetal squames & Vernix caseosa squames & Vernix caseosa  Complications  death due to ARDS, DIC  Complications  death due to ARDS, DIC Dr. Krishna Tadepalli, MD, www.mletips.com
  10. 10. Amniotic Fluid embolism Dr. Krishna Tadepalli, MD, www.mletips.com
  11. 11. Infarction Infarction  Definition = ischemic necrosis of tissue due to occlusion  Definition = ischemic necrosis of tissue due to occlusion of arterial ((in most of cases) or venous ((in gonads) of arterial in most of cases) or venous in gonads) circulation circulation  Most common cause of Death in USA  Most common cause of Death in USA  Most commonly  in 99% of cases = arterial occlusion  Most commonly  in 99% of cases = arterial occlusion by thrombo-embolism by thrombo-embolism  Rarely  venous drainage problem ((in Testis, Ovary)  Rarely  venous drainage problem in Testis, Ovary)  Very rarely  vasospasm  Very rarely  vasospasm  Morphological Types  Red & White  Morphological Types  Red & White  Wedge shaped with base at the periphery of organ  Wedge shaped with base at the periphery of organ  Final outcome Coagulative necrosis ((Liquefactive in  Final outcome Coagulative necrosis Liquefactive in Brain) Brain)  Septic infarction = in pts. With infective Endocarditis  Septic infarction = in pts. With infective Endocarditis Dr. Krishna Tadepalli, MD, www.mletips.com
  12. 12. Infarctions- Types Red (Hemorrhagic) White (Anemic) Red (Hemorrhagic) White (Anemic)  Venous occlusion  Venous occlusion  In loose tissues  In loose tissues (lung) (lung)  Organs with dual  Organs with dual blood supply (Lungs, blood supply (Lungs, Liver) Liver)  Previously congested  Previously congested organs organs ((nutmeg liver) nutmeg liver)  Re- perfused tissues  Re- perfused tissues • Arterial occlusion • Arterial occlusion • Solid organs • Solid organs • End arterial supply • End arterial supply ((Kidney, Spleen, Kidney, Spleen, Retina, Heart) Retina, Heart) Dr. Krishna Tadepalli, MD, www.mletips.com
  13. 13. Hemodynamic Disorders OBJECTIVES Edema Hyperemia and Congestion Hemorrhage Hemostasis and Thrombosis Embolism Infarction Shock Dr. Krishna Tadepalli, MD, www.mletips.com
  14. 14. Infarction Red & White Dr. Krishna Tadepalli, MD, www.mletips.com
  15. 15.  Final outcome of Infarction in heart  Final outcome of Infarction in heart How old is it ( after the onset of MI)? Dr. Krishna Tadepalli, MD, www.mletips.com
  16. 16. Hemodynamic Disorders, Thromboembolic Hemodynamic Disorders, Thromboembolic Disease, and Shock Disease, and Shock OBJECTIVES OBJECTIVES  Edema  Edema  Hyperemia and Congestion  Hyperemia and Congestion  Hemorrhage  Hemorrhage  Hemostasis and Thrombosis  Hemostasis and Thrombosis  Embolism  Embolism  Infarction  Infarction  Shock  Shock Dr. Krishna Tadepalli, MD, www.mletips.com
  17. 17. Shock = Cardiovascular collapse Shock = Cardiovascular collapse • Final common pathway of many disorders • Final common pathway of many disorders ((Hemorrhage, Trauma, Burns, MI, PE, Sepsis) Hemorrhage, Trauma, Burns, MI, PE, Sepsis) • Main Event  Systemic Hypo perfusion ((due to • Main Event  Systemic Hypo perfusion due to ↓cardiac output or effective circulatory volume) ↓cardiac output or effective circulatory volume) •• Types Types – Cardiogenic = MI, Ventricular rupture, PE, etc., – Cardiogenic = MI, Ventricular rupture, PE, etc., – Hypovolemic = Hemorrhage, Fluid loss – Hypovolemic = Hemorrhage, Fluid loss – Septic = most important – Septic = most important – Others = Neurogenic, Anaphylactic ((Type 1 HSR) – Others = Neurogenic, Anaphylactic Type 1 HSR) Dr. Krishna Tadepalli, MD, www.mletips.com
  18. 18. Septic Shock = by Gram +ve bacteria Septic Shock = by Gram +ve bacteria • MCC of mortality in ICU (in USA) • MCC of mortality in ICU (in USA) • Incidence is ↑ ((due to high risk pts., ↑ # of invasive • Incidence is ↑ due to high risk pts., ↑ # of invasive procedures & immuno-compromised pts.) procedures & immuno-compromised pts.) •• Endotoxic shock  MC sub type of septic shock ((70% Endotoxic shock  MC sub type of septic shock 70% of cases), of cases), •• Cause  LPS Cause  LPS •• Super antigens  bacterial proteins cause polyclonal Super antigens  bacterial proteins cause polyclonal activation of T – Lymphocytes activation of T – Lymphocytes –– –– Example ––TSS toxin-1 by Staph. Aureus Example TSS toxin-1 by Staph. Aureus Cause multi organ failure Cause multi organ failure Dr. Krishna Tadepalli, MD, www.mletips.com
  19. 19. Septic shock Endotoxic shock Septic shock Endotoxic shock •• Causes= LPS (Endotoxin = Lipid core and Causes= LPS (Endotoxin = Lipid core and PolySaccharide coat) PolySaccharide coat) •• Effects  Effects  – Low LPS levels  Activate Macrophages  Local – Low LPS levels  Activate Macrophages  Local inflammation  healing inflammation  healing – Moderate LPS levels  ↑cytokines  systemic – Moderate LPS levels  ↑cytokines  systemic effects effects – Higher LPS levels  Septic shock syndrome – Higher LPS levels  Septic shock syndrome •• Mechanism  LPS binds with Circulating Protein  Mechanism  LPS binds with Circulating Protein  later the complex binds with CD 14 All of them later the complex binds with CD 14 All of them finally bind with TLR-4 finally bind with TLR-4 – The interaction on endothelium  ↓anticoagulant – The interaction on endothelium  ↓anticoagulant properties properties – The interaction on Macrophages  ↑ cytokines – The interaction on Macrophages  ↑ cytokines (TNF, IL-1) (TNF, IL-1) Dr. Krishna Tadepalli, MD, www.mletips.com
  20. 20. Shock Dr. Krishna Tadepalli, MD, www.mletips.com
  21. 21. Septic shock syndrome= Multi organ failure Septic shock syndrome= Multi organ failure – 1. Hypotension – 1. Hypotension – 2. DIC – 2. DIC – 3. ARDS – 3. ARDS – 4. Loss of Myocardial Contractility – 4. Loss of Myocardial Contractility •• Stages Stages •• 1. Non – Progressive = compensatory reflex 1. Non – Progressive = compensatory reflex mechanisms ((Baroreceptors, ADH, Catecholamines) mechanisms Baroreceptors, ADH, Catecholamines) •• 2. Progressive = ↓tissue perfusion, Electrolyte 2. Progressive = ↓tissue perfusion, Electrolyte imbalance ((Acidosis, oliguria, Anaerobic glycolysis) imbalance Acidosis, oliguria, Anaerobic glycolysis) •• 3. Irreversible = Tissue injury & Death ((Lysosomal 3. Irreversible = Tissue injury & Death Lysosomal leakage, ↓ Myocardial contractility, Anuria )) leakage, ↓ Myocardial contractility, Anuria Dr. Krishna Tadepalli, MD, www.mletips.com
  22. 22. Septic shock syndrome= Multi organ failure Septic shock syndrome= Multi organ failure •• Organ damage Organ damage Brain  Ischemic encephalopathy Brain  Ischemic encephalopathy Heart  Necrosis, Contraction bands Heart  Necrosis, Contraction bands Kidney  ATN Kidney  ATN Lungs  Shock lungs Lungs  Shock lungs GIT  Hemorrhagic Enteropathy GIT  Hemorrhagic Enteropathy Liver  Fatty change, Hemorrhagic Necrosis Liver  Fatty change, Hemorrhagic Necrosis •• Clinical features useful in diagnosis Clinical features useful in diagnosis –– Septicemic shock  skin is warm in early stages Septicemic shock  skin is warm in early stages ((Vasodilatation Vasodilatation –– Hypovolemic or Cardiogenic shock  cool, calmy, cyanotic Hypovolemic or Cardiogenic shock  cool, calmy, cyanotic skin ((due to Hypotension) skin due to Hypotension) Dr. Krishna Tadepalli, MD, www.mletips.com

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