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![Parameters that affect outcome after infection. The natural evolution of a systemic inflammatory
disorder or a sepsis is greatly influenced by parameters linked to the pathogen(s), the ICU treatments
and by many others elements associated with the patient. [Cavaillon & Adrie – IN Sepsis and Non-
infectious Systemic Inflammation: From Biology to Critical Care, Wiley Sept. 2008]](https://image.slidesharecdn.com/polytraumapart4sepsis-190118151942/75/Polytrauma-part-4-SEPSIS-59-2048.jpg)
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Polytrauma part 4 (SEPSIS)
The document discusses the complexities of septic shock and multi-organ dysfunction syndrome (MODS) in polytrauma patients, highlighting the phases of trauma mortality and the immune system's response to sepsis. It outlines the importance of early detection and treatment, emphasizing the critical role of timely interventions like antibiotics and fluid resuscitation in improving patient outcomes. The text also details the mechanisms by which infections can lead to sepsis, as well as the risk factors and clinical criteria associated with its progression.
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Polytrauma part 4 (SEPSIS)
- 1. Dr. Fathi Neana,MD Chief of Orthopaedics Dr. Fakhry & Dr. A. Al-Garzaie Hospital January, 18 - 2019 Polytrauma Part 4 Septic Shock
- 3. Trauma Mortality (3Peaks) FIRST PEAK (24 hours) Early phase - immediate death severe brain injury, disruption of great vessels, cardiac disruption Second phase – within 24 hours subdural, epidural hematomas, hemopneumothorax, severe abdominal injuries, multiple extremity injuries (bleeding) SECOND PEAK (2-7 Days) Acute Respiratory Distress Syndrome (ARDS) 40 - 50% Mortality THIRD PEAK – DELAYED ( < 7 Days) Multisystem organ failure, Sepsis (Septic Death) 28% Mortality
- 5. Trauma Tissue injury Infection Inflammatory Mediators Release Organ Injury Multi organ(Dysfunction –Failure) Syndrome (MODS – MOF) Common Pathological Pathways The immune response 1- Inflammatory mediators ->> Systemic inflammatory response syndrome (SIRS ) 2- Anti-inflammatory mediators ->> Compensatory anti-inflammatory response syndrome (CARS) 3- The conflict between these two immune responses (SIRS) vs. (CARS) will end up with: A- Cure B- Death (Parenchymal cell Necrosis and Apoptosis ) C- Long standing inflammation ->> Multi organ Dysfunction Syndrome (MODS ) or Failure (MOF)
- 6. SIRS With sepsis immuneresponse and haemostatic response amplify each other MODS DIC Circulating mediators Circulating mediators Haemostatic Response Immunological Response ModificationModification AmplificationAmplification Ischaemia -Ischaemia - BleedingBleeding DestructionDestruction
- 7. With sepsis immuneresponse and haemostatic response amplify each other
- 8. Sepsis is thesystemic inflammatory response syndrome (SIRS) due to severe infection Micro-organisms grow out of control => hyperinflammatory response With this insidious pathology the body attacks itself (auto immunity) => life threatening risk of organ dysfunction, septic shock and death Micro-organisms can invade the body through wounds, IV lines, catheters etc Infection does not mean Sepsis
- 9. Figure 1: Relationshipbetween systemic inflammatory response and infection, where the overlap indicates sepsis SIRS: Systemic inflammatory response syndrome Septic shock Sepsis Sever Sepsis
- 10. The Vicious Cycleof Inflammation and Coagulation Sepsis SIRS 2nd to infection Septic shock Hypoperfusionor organdysfunction Refractory hypotension DIC Severe sepsis
- 11. MODS - MOF(Multi Organ Dysfunction or Failure Syndrome)
- 12. Septic shock, Multisystemorgan failure and Septic Death are a Constant threat in polytrauma patient Trauma Mortality Third Peak of death < 7 Days 28% Overall mortality in poly trauma Mortality from MODS due to Sepsis 30%-70% Sepsis, Sever Sepsis and Septic shock A race to Death between Host immune system & Pathogens Sepsis Kills more than 210,000 people in the US annually Sepsis Kills about 1,400 people worldwide every day
- 13. Severe sepsis is theleading cause of death in the non- Coronary ICU Sepsis has very low Standard of Care in hospitals The graph shows, more people die each year in the USA of severe sepsis and septic shock than many other major diseases
- 14. Sepsis before onecentury • Infection was a major problem during surgery • People died after surgery from the infection • Compound (open) fractures almost always ended in death because of infection (Operative treatment only after failure of repeated conservative trials) Alexander Fleming (1881-1955) - Penicillin 1928 - Nobel Prize 1945 Dr. Gerhard Domagk (1895-1964) Sulfa drugs 1935 - Nobel Prize 1939
- 15. Antibiotic Grouping ByMechanism
- 16.
- 17. Bacterial infections arethe most common Begin by invasion => growth out of control => hyper inflammatory response Result from something seemingly harmless as a scraped knee or nicked cuticle or from a more serious medical problem such as appendicitis, pneumonia, meningitis, urinary tract infection, osteomyelitis In hospitalized patients, common sites include IV lines, surgical incisions, urinary catheters and bed sores Causes of Sepsis
- 18. G-ve Bacilli endotoxins: 2 G+ve Bacilli : 1 E.coli, klebsiella, proteus, bactroids, psuedomonas Genito-urinary tract the most common site Wounds, IV lines, Catheters, sores, etc Causes of Sepsis
- 19. Two main typesof bacterial toxins 1- Endotoxins lip polysaccharide (LPS) or lipooligosaccharide (LOS) which are associated with the cell wall of Gram-negative bacteria 2- Exotoxins Proteins which are released from bacterial cells and act at tissue sites remote from the site of bacterial growth Bacterial Toxigenesis
- 20. Endotoxins : LPS– LOS
- 21.
- 22. Necrotizing Fasciitis -flesh eating bacteria 1- Mainly virulent group A beta hemolytic streptococcus 2- Enterobacteriaceae a large family of gram negative, non- spore forming rods, which are facultative anaerobe anaerobes include: bacteroides fragilis Peptostreptococcus clostridium species aerobes include: staph aureus escherichia coli
- 23. Gas gangrene -Clostridium perfringens
- 24. Tetanus - Clostridiumtetani
- 25. Highly characteristic abnormal,sustained spasm of facial muscles Sign of Tetanus & poisoning with Strychnine Risus Sardonicus
- 26.
- 27. •Immune compromised peopledue to Illnesses as HIV/AIDS or Cancer Drugs (to prevent rejection of transplanted organs – corticosteroids) •Very young babies and The elderly with other health problems •Hospitalized people with an invasive medical procedures • Uncontrolled Diabetes Sepsis Risk Factors Uncontrolled Diabetes Osteomyelitis
- 28.
- 29.
- 30. -Adult human have60,000 miles (96,560 km) of capillaries - Surface area 800–1000 m2 (an area greater than three tennis courts) - How the total volume of this system is roughly 5 liters, same as the total volume of blood ? If the heart and major vessels are to be kept filled, all the capillaries cannot be filled at once So a continual redirection of blood from organ to organ takes place in response to the changing needs of the body For example: During vigorous exercise,capillary beds in the skeletal muscles open at the expense of those in the viscera. The reverse occurs after a heavy meal The Capillary Bed
- 31. The Capillary Bed Thewalls of arterioles are encased in Smooth Muscles. Constriction of arterioles decreases blood flow into the capillary beds they supply while dilation has the opposite effect.. These actions are carried out by the autonomic nervous system
- 32.
- 33. Acute disruption ofcirculatory function, resulting in Insufficiency of tissue perfusion, oxygen utilization and cellular energy producion (? skeletal muscles – lactic acid) Low BP is NOT sine qua non of shock What ‘type of shock’ is septic shock? Septic shock has the features of: 1- Hypovolemic shock 2- Cardiac shock 3- Distributive shock What is shock?
- 34. Capillary beds mayopen without others closing in compensation. (maldistribution) The volume of blood remains unchanged while The blood pools in the capillary beds. (relative hypovolaemia). The Blood pressure declines abruptly and If untreated shock is usually fatal Hypovollemic Shock can also result from severe bleeding The heart can only pump as much blood as it receives. If insufficient blood gets back to the heart, its output — and hence blood pressure — drops. (Cardiogenic). The tissues fail to receive enough oxygen. This is especially critical for the brain and the heart itself To cope with the problem, arterioles constrict and shut down the capillary beds — except those in the brain and heart. This reduces the volume of the system and helps maintain normal blood pressure Septic shock has the features of: 1- Hypovolemic shock 2- Cardiac shock 3- Distributive shock What ‘type of shock is septic shock?
- 35. Septic shock Pathological Pathway 1-Endo toxins (LPS – LOS) 2- Vasoconstriction + DIC 3- Tissue anoxia => Lactic acid production 4- Metabolic acidosis (Lactic acid) 5- Vasodilatation => Stagnant anoxia 6- Tissue necrosis => Capillary damage => Fluid loss 7- Hypovolaemia 8- Septic shock 9- MODS and MOF 10- Septic death
- 36. Tissue anoxia andLactic acid production
- 37. Tissue anoxia andLactic acid production
- 38. Multi organ Dysfunction–FailureSyndrome (MODS – MOF) Defined as the development of potentially Reversible (Irreversible) physiologic derangement involving two or more organ systems
- 39. Multi organ Dysfunction–FailureSyndrome (MODS – MOF) Pulmonary Failure of gas exchange V/Q mismatch Volutrauma Barotrauma Late ARDS Renal Oliguria Elevated creatinine Fluid and electrolyte abnormalities Anuria Cardiovascular Hypotension Myocardial depression GI/Hepatic Elevated clotting times Elevated bilirubin Intolerance to feedings Neurologic Altered level of consciousness Hematologic Thrombocytopenia Leukocytosis Leukopenia Anemia Immunologic Nosocomial infections Delayed type hypersensitivity Altered production of antibodies Abnormal regulation of lymphocytes Endocrine Hyperglycemia Sick euthyroid syndrome Adrenal insufficiency
- 40. Early detection and treatmentof severe sepsis
- 41. Evaluating Severe Sepsis(3 Yes) Q1: Suspected infection Clinical judgment to determine if there is a new potential site of infection Q2: Signs of SIRS Two signs & symptoms of SIRS based on vitals and recent lab results Q3: Organ dysfunction Often discovered by an abnormal serum lactate value Early recognition is The key!
- 42. Adult Sepsis clinicalCriteria Sepsis SIRS due to infection Diagnosed Clinically Positive cultures add to the validity but not required for diagnosis Severe Sepsis Sepsis Plus signs of hypo perfusion or organ dysfunction Not explained by other known etiology of organ dysfunction Septic Shock Severe sepsis Plus Refractory hypotension (BP<90/60) despite adequate fluid resuscitation and/or a serum lactate level >4.0 mmol/L
- 43. Hyperthermia >38.3°C or Hypothermia<36°C Acutely Altered Mental Status Tachycardia >90 bpm Tachypnea RR > 20 or PaCO2 < 32 Leukocytosis (>12,000 µL-1( or Leukopenia (<4,000 µL-1( or >10% bands Hyperglycemia (>120 mg/dl) in the absence of diabetes Signs of Sepsis (SIRS)
- 44. Hypotension (<90/60 orMAP <65( Lactate >2 Areas of mottled skin or capillary refill >3 seconds Creatinine >2.0 mg/dl Disseminated intravascular coagulation (DIC( Platelet count <100,000 Acute renal failure or urine output <0.5 ml/kg/hr for at least 2 hours Hepatic dysfunction as evidenced by Bilirubin >2 or INR >1.5 Cardiac dysfunction Acute lung injury or ARDS Signs of severe sepsis SIRS + hypoperfusion or organ dysfunction (MODS)
- 45. Inflammatory triad Fever shakingchills Tachycardia flushed skin Signs of hypoperfusion Altered sensorium Urine output, jaundice >CFT (Complement Fixation Test ) Wide pulse pressure ..bounding pulses Warm Shock Signs of Hypotension Cold and clammy skin Mottling Tachycardia Cyanosis Hypoxemia Acidosis Lactate >4 Narrow pulse pressure Cold shock Signs of septic shock SIRS + MODS + HYPOTENSION < 90/60 mmHg
- 46. Defining the septicpicture (Brook Sepsis Recognition)
- 47. Staging of SepticShock Recognize septic shock early by Clinical judgment and High index of suspicions: I.Compensated / Preshock / Hyperdynamic II.Decompensated / Organ hypoperfusion III.End organ failure / Irreversible Antibiotics, Fluid replacement , ? Corticosteroids, Metabolic acidosis, Dopamine infusion Don't wait for +ve blood culture Do not wait for the BP to fall ! • Lower limit for systolic BP = 70 + ( age x 2)
- 48. Don't wait for +veblood culture Do not wait for the BP to fall !
- 49. Treatment of Sepsis,Sever Sepsis & Septic shock Pathological Pathway guide the treatment Antibiotics Fluid replacement Ventilation Metabolic acidosis Dopamine infusion (Vasopressor) ? Corticosteroids 1- Endo toxins (LPS – LOS) 2- Vasoconstriction + DIC 3- Tissue anoxia => Lactic acid production 4- Metabolic acidosis (Lactic acid) 5- Vasodilatation => Stagnant anoxia 6- Tissue necrosis => Capillary damage => Fluid loss 7- Hypovolaemia 8- Septic shock 9- MODS and MOF 10- Septic death
- 50. 35Y M. ISS41 MRSA infected open fracture lt femur With (SIRS) and (MODS) (sever sepsis)
- 51. Picture 1: Cellulitis,an infection of the skin, may lead to sepsis, particularly in elderly people and those with diabetes or other illnesses that alter the immune system Picture 2: This rash, showing petechia and purpura, may be a sign of bacteria in the bloodstream (bacteremia)
- 52. Treatment of Sepsis,Sever Sepsis & Septic shock Pathological Pathway guide the treatment 1- Control infection source (Damage control) 2- Antibiotics 3- Volume resuscitation (30cc/kg NS) 4- Vasopressor support after volume loading 5- Low volume ventilation 6- Nutritional support 7-Dialysis No proven benefit from steroids , anti-inflammatories Transfusion for Hemoglobin > 7 Increasing Delivered O2 (DO2) Activated Protein C (natural anticoagulant in DIC)
- 53. Protein C inseptic patients • The plasma concentration of Proein C is reduced in septic patients due to: – Capillary leak – Degradation by elastase – Decreased synthesis – Increased consumption during DIC • Activation of PC is compromised in septic patients because the endothelial expression of thrombomodulin and endothelial protein C receptor is suppressed
- 54. • 3-hour Bundle– Actions to be taken within the first 3 hours of resuscitation from initial recognition for adults and within 60 minutes from initial recognition for pediatric patients. • 6 – hour Bundle – Actions to be taken within the first 6 hours of resuscitation from initial recognition for adults and within 60 minutes from initial recognition for pediatric patients. Best Practice Treatment of Severe Sepsis Two treatment track – invasive or non-invasive Track followed is based on the criticality and initial response to hemodynamic measures Resuscitation Bundles 3-hour and 6-hour Bundle Division
- 55. •Serum lactate •Blood cultures •Additionalcultures potential site of infection •Antibiotic administration early and appropriate broad-spectrum antibiotic within 3 hour for ED presentation. within 1 hour for floors/ICU presentation •Fluid replacement hypotension and/or lactate >4 mmol/L A minimum of 30 ml/kg of fluids in adults and 20mL/kg of fluids in children. Resuscitation Bundle 3-hour Bundle
- 56. • Vasopressor therapy forpersistent hypotension (mean arterial pressure MAP <65 in adults) despite initial fluid administration • Re-measure lactate if the initial value was elevated • Invasive A central venous catheter capable of measuring CVP • Non-invasive Contraindications for invasive track Trending of lactate levels to gauge fluid response Resuscitation Bundle 6-hour Bundle
- 57.
- 58. Sepsis simply isa Race to death between the host immune system and the pathogens Sepsis, (SIRS due to severe infection) kills more than 210,000 people in the US /year kills about 1,400 people worldwide every day Significant decrease in Mortality due to increased Recognition and early Treatment Severe Sepsis Treatment Reliability and Mortality The key behind successful treatment is ! 1- Early recognition by Clinical judgment 2- Recognize septic shock by High index of suspicions 3- Start Early treatment
- 59. Parameters that affectoutcome after infection. The natural evolution of a systemic inflammatory disorder or a sepsis is greatly influenced by parameters linked to the pathogen(s), the ICU treatments and by many others elements associated with the patient. [Cavaillon & Adrie – IN Sepsis and Non- infectious Systemic Inflammation: From Biology to Critical Care, Wiley Sept. 2008]
- 60. Early Detection andTreatment of Severe SepsisConfidential and required to be collected and maintained pursuant to Public Health Law sections 2805-j k l and m Significant decrease in Mortality for ED presentations & In-patient units due to increased recognition and early treatment
- 64.
Editor's Notes
- #4 First phase is immediate death or shortly thereafter due to severe brain injury, or disruption of the heart, aorta, or great vessels. Second phase: Death occurs minutes to a few hours. Deaths are due to lifethreating injuries such as subdural, epidural hematomas, hemopneumothoraces, severe abdominal injuries, long bone fractures, multiple injuries associated with blood loss. This is the group that with rapid evacuation , resuscitation and proper early management can be given the best chance for survival and improved outcomes. Third phase: Patients die days to weeks from multiple system organ failure and sepsis. Specialized centers with their expertise and experience can reduce mortality in the second and third phases
- #13 First phase is immediate death or shortly thereafter due to severe brain injury, or disruption of the heart, aorta, or great vessels. Second phase: Death occurs minutes to a few hours. Deaths are due to lifethreating injuries such as subdural, epidural hematomas, hemopneumothoraces, severe abdominal injuries, long bone fractures, multiple injuries associated with blood loss. This is the group that with rapid evacuation , resuscitation and proper early management can be given the best chance for survival and improved outcomes. Third phase: Patients die days to weeks from multiple system organ failure and sepsis. Specialized centers with their expertise and experience can reduce mortality in the second and third phases
- #36 First phase is immediate death or shortly thereafter due to severe brain injury, or disruption of the heart, aorta, or great vessels. Second phase: Death occurs minutes to a few hours. Deaths are due to lifethreating injuries such as subdural, epidural hematomas, hemopneumothoraces, severe abdominal injuries, long bone fractures, multiple injuries associated with blood loss. This is the group that with rapid evacuation , resuscitation and proper early management can be given the best chance for survival and improved outcomes. Third phase: Patients die days to weeks from multiple system organ failure and sepsis. Specialized centers with their expertise and experience can reduce mortality in the second and third phases
- #42 The Society for Critical Care Medicine developed a screening tool for the evaluation of a septic patient. If all three questions are answered “yes,” the patient meets the criteria for Severe Sepsis and should begin treatment. Both date and time of presentation are noted for accurate reporting.
- #61 Our 2006 baseline period provided a hospital-wide sepsis mortality rate of nearly 26 deaths per 100 discharges. Despite overall improvements throughout the proceeding years and significant progress in our Emergency Department, our inpatient units remained near baseline. Use of the alert has increased our capture rate on these inpatient units while ensuring earlier recognition and timely treatment has decreased our mortality rate to below 20 deaths per 100 discharges.