sepsis

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sepsis

  1. 1. Sepsis syndrome Dr sanjay sharma Specialist a&e
  2. 2. A 73-year-old woman is brought to the emergency center from an assistedlivingfacility. The patient has a history of dementia, hypertension, and type IIdiabetes mellitus. By report, she has had chills and a productive cough forseveral days. In the past 24 hours she has become weaker and does not want toget out of bed. The physical examination reveals a thin, elderly woman who issomnolent but arousable. Her rectal temperature is 36.0°C (96.8°F), pulse rateis 118 beats per minute, blood pressure is 84/50 mm Hg, and respiratory rateis 22 breaths per minute. Her mucous membranes are dry. Her heart istachycardic but regular. She has crackles at her right lung base with a scantwheeze. Her abdomen is soft and non tender. The extremities feel cool and herpulses are rapid and thready. The patient is moving all extremities, withoutfocal deficits.What is the most likely diagnosis?
  3. 3. Systemic inflammatory response syndrome (SIRS)• At least two of the following conditions:1. Oral temperature of >38 or <352. Respiratory rate of > 20 breaths/min.3. Heart rate of > 90/min.4. Wbc count of > 12000 or < 4000
  4. 4. Sepsis syndrome• Represents the systemic inflammatory response triggered by an infection in the host and is mediated by chemical messengers.• Tachycardia, tachypnea,fever, and immune system activation are manifestations.• Cellular injury, tissue damage, shock, multiorgan failure or death results if body is unable to overcome this insult.
  5. 5. sepsis• SIRS that has a proven or suspected microbial source.• Severe sepsis: sepsis with one or more signs of organ dysfunction1. Hypotension or hypoperfusion.2. Metabolic acidosis.3. Acute alteration in mental status.4. Oliguria5. Adult respiratory distress syndrome.
  6. 6. Septic shock• Sepsis with hypotension that is unresponsive to fluid resuscitation plus organ dysfunction or perfusion abnormalities.• Metabolic acidosis. (lactic acidosis).• Alteration in mental status.• Oliguria.• Adult respiratory distress syndrome.
  7. 7. Multiple organ dysfunction syndrome (MODS).• Dysfunction of more then one organ, requiring intervention.• Clinical progression from SIRS – to sepsis- to severe sepsis- to septic shock-MODS.• MORTALITY RATE INCREASES WITH SEVERITY OF SEPSIS.
  8. 8. BACTEREMIA• Presence of viable bacteria in the blood , as evidenced by positive blood culture.• Positive blood culture are not essential in the diagnosis of sepsis.• Culture positive and culture negative septic patients have similar outcome.• In recent prospective studies only 17% of pts with sepsis, 25% of pts with severe sepsis and 69 % of pts with septic shock had positive blood culture.
  9. 9. sepsis• Pneumonia ,abdominal abscess, viscus perforation, pyelonephritis are primary causes of sepsis.• Gram positive accounts for 25 to 50%,• Gram negative 30 to 60 %• Fungi : 2 to 10 %.
  10. 10. Common organism• E.coli, staph aureus, pseudomonas, enterococcus faecalis, streptococci pnemoniae, klebsiella pnemoniae, and coagulase negative staphylococcus.
  11. 11. Host factor• Elderly patients• Chemotherapy induced neutropenia.• AIDS.• STEROID DEPENDENCY• Indwelling device such as• Intravascular catheter,• Prosthetic device• Et tube• Increases susceptibility to sepsis
  12. 12. epidemiology• Sepsis is 10th common cause of death in usa.• 7,51,000 new cases of sepsis estimated per year in united states.• Cost of caring for septic patients is estimated 17 billion us dollars/year .• Sepsis accounts for 2 to 10 cases per 100 hospital admission.• Mortality rate from sepsis are estimated from 20 to 50 %.
  13. 13. pathophysiology• Sepsis is the endpoint of a complex process that begins with an infection.• Initial host response is to mobilize inflammatory cells , particularly neutrophils and macrophages, to the site of infection.
  14. 14. pathophysiology• Inflammatory cells release cytokines,• If Inflammatory mediators are not regulated sepsis will occur.
  15. 15. pathophysiology• In the setting of ongoing toxin release, persistent inflammatory response occurs with ongoing mediator activation, cellular hypoxia, tissue injury, shock, multiple organ failure, and potentially death.
  16. 16. pathophysiology• Gram negative sepsis is initiated by endotoxin ,a lipopolysaccharide component of bacteria cell wall.
  17. 17. Gram positive organism• Produce inflammatory response by direct action of its cell wall components and indirect action of secreted soluble substance.
  18. 18. Gram positive organism• Cellular wall components such as peptidoglycan.• exotoxin are substance secreted by bacteria that produce host response through cell membrane receptors.
  19. 19. Mediators of sepsis• In response to toxins, the body reacts by secreting substance such as cytokines, eicosanoids, platelet activation factor, oxygen free radicals, complement and fibrinolysins.
  20. 20. Mediators of sepsis• Six categories of cytokines exists:• Interleukins 6 &8, tumor necrosis factor, interferon, colony stimulating factor, chemotactic factor, transforming growth factor beta.
  21. 21. cytokines• Cytokines are primarily pro and anti inflammatory or growth promoting.• The main pro-inflammatory cytokines are IL-1 , TNF, AND IL-8.• Primary anti-inflammatory cytokines are IL-10, IL-6, transforming growth factor beta.
  22. 22. Inflammatory response• If inflammatory response is adequate , infection is controlled.• If response is deficient or excessive, persistent and worsening cascade is produced leading to shock, organ failure and potentially death.
  23. 23. Organ system dysfunction• Neurologic• Patient with sepsis, manifested by• Altered mental status• Lethargy• Septic encephalopathy.
  24. 24. Organ system dysfunction• Mortality rate is higher if gcs less then 13• Causes are endotoxemia, renal hepatic dysfunction, altered cerebral perfusion, metabolic derangement.
  25. 25. Cardio vascular dysfunction in sepsis• Myocardial depression• Distributive shock
  26. 26. Cardio vascular dysfunction in sepsis• Early in sepsis hyperdynamic state causes increased cardiac output, and decreased systemic vascular resistance.• Aggressive fluid resus increases pre load and ejection fraction.• Cardio vascular compromise from septic shock is reversible and normal function returns with in 10 days.
  27. 27. Pulmonary compromise• Is common and often lethal.• Common pulmonary end point is ARDS• Bilateral pulmonary infiltrates on frontal chest xray.• Impaired oxygenation• Arterial hypoxemia• Alveolar-capillary damage.
  28. 28. Gastro intestinal• Prolonged ilieus due to hypoperfusion• Blood flow dependant on mean arterial pressure.• Little auto regulation of blood flow• Liver produces some of the mediator of sepsis• Aminotranferase and bilirubin are raised early in sepsis.
  29. 29. Endocrine• IL-1 and IL-6 both activate hypothalamic-pituitary axis.• TNF depress pituitary function.• Adrenal insufficiency due to decreased blood flow in sepsis• Decreased pituitary secretion of ACTH due to severe stress.
  30. 30. Hematologic• SEPSIS causes abnormalities in coagulation.• Endotoxin, TNF, IL-1, protein C, protein S, and fibrinolysin leads to consumption of essential factors leading to DIC.• Activation of coagulation cascade leads to thrombi, if not corrected compromise organ perfusion and contributes to organ failure.
  31. 31. Clinical features• Septic patient manifests signs of Infection• TACHYCARDIA• TACHYPNEA• HYPERTHERMIA OR HYPOTHERMIA• HYPOTENSION IF SEVERE SEPSIS
  32. 32. CLINICAL FEATURES• Early signs of sepsis tachycardia and tachypnea.• Septic patient have flushed skin with warm extremities due to early vasodilatation and hyperdynamic state.• Severe septic shock skin appears to be mottled and cyanotic .
  33. 33. Septic shock• Should be differentiated from hypovolemic or cardiogenic shock• Septic patient will classically appear flushed with warm well perfused extremities,• In hypovolemic or cardiogenic shock patient will appear cool clammy with poorly perfused extremities. Neck veins flat, pulse rapid and thready.
  34. 34. Risk factors for sepsis• Immunocompromised state• AIDS• DIABETES• SPLENECTOMY• CONCURRENT CHEMOTHERAPY• ELDERLY AGE.
  35. 35. RESPIRATORY SYSTEM• Most common focus of infection• Productive cough, fever , chills, urti, throat and ear pain.• Both presence of pnemonia, tachypnea, hypoxia are predictors of death in sepsis• Look for focal infection , exudative tonsillitis, dullness on lung auscultation, pharngeal thrush as marker of immuno compromised state.
  36. 36. Gastro intestinal system• Second most common source of sepsis• h/o abdominal pain, nausea, vomiting, diarrhea, fever should be noted.• Physical examination to r/o peritoneal irritation, abdominal tenderness, hyperactive or hypoactive bowel sounds is critical to find source of sepsis.
  37. 37. Physical findings• Murphys sign indicating cholecystitis• Mcburneys point tenderness indicating appendicitis.• Left lower quadrant pain suggesting diverticulitis• Rectal examination revealing rectal abscess or prostatitis
  38. 38. Neurologic• Signs of meningitis• Nuchal rigidity• Fevers• Change in consciousness• Lethargy• Altered mental status may be due to Neurologic disease or due to decreased perfusion from a shock state.
  39. 39. Genitourinary• History of flank pain• Dysuria• Polyuria• Discharge• Foley catheter placement• Genitalia should be evaluated for ulcer, discharge, penile or vulvar lesion.• Rectal examination to r/o rectal abscess, tender boggy prostrate t/ r/o prostatitis
  40. 40. Musculoskeletal• Redness swelling and warmth over joint• Decreased ROM of joint• Cellulitis• Abscess• Wound infection• Fasciitis• Crepitus indicates gas forming organism• Lymphadenopathy,
  41. 41. Diagnostic strategy hematology• White blood cells marker of inflammation• Leucocytosis• Febrile neutropenic patient are at risk of increased severe infection
  42. 42. Diagnostic strategy hematology• WBC < 500 cells/ cubic mm should be admitted, isolated and iv antibiotics• Hemoglobin Hb > 10 and haematocrit HCT > 30 % should be maintained
  43. 43. DIC• Thrombocytopenia• Elevated prothrombin time• Elevated activated partial thromboplastin time.• Decreased fibrinogen• Increased fibrin split products.• Are associated with DIC and severe sepsis syndrome
  44. 44. chemistry• Low bicarbonate level suggests acidosis and inadequate perfusion• Elevated anion gap acidosis represent lactic acidosis or diabetic ketoacidosis.• High creatinine level : renal dysfunction• Elevated Lactate level: poor prognosis• Elevated amylase and lipase : pancreatitis• LFT : to identify liver failure
  45. 45. microbiology• Blood, sputum, urine, csf , tissue culture are important to identify organism• Gram stain of sputum, csf, abscess, help early prediction of organism• Urinalysis showing Leucocytosis : UTI• CSF Leucocytosis : meningitis
  46. 46. radiology• Chest xray : focal infiltrate : pneumonia• Fluffy bilateral infiltrate : ARDS• upright chest x ray : to r/o gas under diaphragm , suspected bowel perforation• Pneumomediastinum : esophageal perforation, mediastinitis• Soft tissue x ray of infected area : looking for air , TO r/o gas forming organism
  47. 47. CT SCAN• Diverticulitis, appendicitis, necrotizing pancreatitis, micro perforation of stomach or bowel , intra abdominal abscess best diagnosed by CT scan• MRI scan to identify soft tissue infection , necrotizing Fasciitis or epidural abscess.• USG for cholecystitis, tubo ovarian abscess.
  48. 48. Differential consideration for sepsis• Dehydration • DIC• Acute respiratory • Anaphylaxis distress syndrome • Diabetic ketoacidosis• Anemia • Burns• Ischemia• Hypoxia • Heat exhaustion• CCF • Trauma• Vasculitis • Blood loss• pancreatitis • Cardiac contusion
  49. 49. Differential consideration for septic shock• Hypovolemic shock • Vasogenic shock• Acute blood loss • Anaphylaxis• Severe dehydration • paralysis• Cardiogenic shock• Pulmonary embolus• Myocardial infarction• Pericardial tamponade• Tension pneumothorax
  50. 50. Management of sepsis• Early detection and aggressive management reduces mortality.• Primary goal :Adequate tissue oxygenation and perfusion .• AIRWAY management, intravenous access, oxygen, antibiotics, fluid resuscitation .
  51. 51. Resus in emergency dept• Early fluid resus,• Normalization of blood pressure• Adequate oxygen delivery• Proper tissue oxygenation• In septic shock bp <90, fluid challenge 20- 30 ml/kg or lactic acid > 4 mmol/l• Aim is to normalize preload and to prevent hypoxia
  52. 52. preload• Patient in sepsis or septic shock are often in a state of fluid deficit.• On an average 5 liters of fluid are needed in first 6 hours of resuscitation.• CVP should be maintained at a level of 8- 12 mm hg .• Intubated patient with positive pressure ventilation the level should be 12-16 mm Hg
  53. 53. PERFUSION PRESSURE• AIM is to maintain an adequate blood pressure.• Mean arterial pressure ( 2/3 diastolic+ 1/3 systolic) should be kept between 60-90 mm Hg.• IF mean arterial pressure is below 60 mm Hg in the presence of adequate preload , vasopressor should be started.
  54. 54. Oxygen delivery• Once preload and pressure is normalized• Focus should be on oxygen delivery
  55. 55. Oxygen delivery• Hemoglobin should be maintained 8-10 g/dl, haematocrit of 30%.• Oxygen delivery by non rebreather mask or intubation,• If this is normalized , and patient not tachycardia, doputamine can be added to increase cardiac contractility and increase cardiac output resulting improved oxygen delivery
  56. 56. Respiratory support• Patients with respiratory rate >30 are likely to develop respiratory collapse.• 85 % of pts with severe sepsis needs mechanical ventilation.• Improved oxygen delivery is achieved by mechanical ventilation, sedation and paralysis.
  57. 57. Intubation guidelines• Hypercapnia• Persistent hypoxemia• Airway compromise• Profound acidosis• Intubation and mechanical ventilation provide positive pressure ventilation .
  58. 58. Cardio vascular support fluid resus• Pts with sepsis require large volume of iv fluid to maintain perfusion.• Intra vascular Hypovolemia is due to vasodilatations and diffuse capillary leak.• 6-10 liters of crystalloid may be required in first 24 hours.
  59. 59. Fluid resus• Fluid replacement must be • NORMAL SALINE and titrated to clinical ringer lactate are equally parameter such as: effective and neither• Heart rate worsens lactic acidosis• Blood pressure• Change in mental status • Colloids are as effective as• Capillary refill crystalloids• Cool skin• Urine output(0.5-1 • Colloids are expensive ml/kg/hr)
  60. 60. vasopressor• If fluid resus fails ,. Vasopressor support may be required• Septic patient requiring vasopressor should have an arterial cannula so that blood pressure can be monitored more accurately• Mean arterial pressure should be maintained 60-70 mm Hg.
  61. 61. Dosing of vasopressor• DRUG DOSE• Dobutamine 5-15 micro gm/kg/min• Dopamine 2-20 micro gm/kg/min• Epinephrine 5-20 micro gm/kg/min• Phenylephrine 2-20 micro gm/kg/min• Norepinephrine 5-20 micro gm/kg/min
  62. 62. Management recommendation for hemodynamic support• Basic principle• Admission to ICU• Arterial cannulation in pts with shock• Resus to target tissue perfusion• Central venous or pulmonary arterial catheter placement to assess cardiac filling.
  63. 63. Fluid resus• Fluid are primary modality to resus• Colloids and crystalloids equally effective• Invasive monitoring for patients not responding to initial resus with target pulmonary wedge pressure of 12-15 mm hg• HB concentration should be maintained 8- 10 g/dl
  64. 64. Vasopressor therapy• Dopamine is first line agent in shock unresponsive to fluid resus• Routine low dose dopamine is not recommended• Epinephrine is reserved for refractory shock.• Vasopressin may be considered in refractory shock not responding to fluid resus and other vasopressor.
  65. 65. Inotropic therapy• Dobutamine is the first choice for pts with refractory low cardiac index• Dobutamine may improve cardiac index and organ perfusion• Vasopressor and inotropes can be titrated separately to maintain mean arterial pressure• Epinephrine and dopamine can be used as inotropes.
  66. 66. antibiotics• Antibiotics should target nidus of infection.• Mortality is reduced by 50 %• If pts condition permits , culture before starting antibiotics.• Double cover for virulent organism such as pseudomonas.aeruginosa and• Multiple organism infection such as peritonitis
  67. 67. Suggested antibiotics• Pneumonia: 2nd or 3rd generation cephalosporin• Abdominal infection :ampicillin + amino glycoside + metronidazole• Urinary : 3rd generation cephalosporin or ampicillin + aminoglycoside.• Cellulitis: cefazolin,
  68. 68. Suggested antibiotics• if MRSA : add vancomycin• CSF: ceftriazone+ vancomycin• Iv drug abuse: nafcillin +aminoglycoside
  69. 69. Steroid therapy• random cortisol level should be measured in the emergency dept , to guide inpatient therapy ,• If steroid administered , it should be low dosed < 300mg/day of hydrocortisone.
  70. 70. disposition• Pts with sepsis syndrome should have consultation with admitting service while in emergency dept.• Once emergency dept management is complete , antibiotics are given, need for emergency operative intervention and procedure has been excluded,• Patient should be admitted.
  71. 71. disposition• Pts with severe sepsis and septic shock , MODS should be admitted to ICU• Pts with SIRS can be admitted in high dependency ward monitored with closed supervision .
  72. 72. Key concepts• Sepsis is a progression of disease ranging from SIRS to sepsis to severe sepsis to septic shock to MODS.• Elderly, Immunocompromised, neutropenic pts are at increased risk for development of sepsis syndromes.
  73. 73. Key concepts• Early administration of appropriate antibiotics is essential in the treatment of sepsis syndromes.• Patients with septic shock should be treated with aggressive fluid resuscitation and vasopressor therapy as needed.
  74. 74. Thank You
  75. 75. A 73-year-old woman is brought to the emergency center from an assistedlivingfacility. The patient has a history of dementia, hypertension, and type IIdiabetes mellitus. By report, she has had chills and a productive cough forseveral days. In the past 24 hours she has become weaker and does not want toget out of bed. The physical examination reveals a thin, elderly woman who issomnolent but arousable. Her rectal temperature is 36.0°C (96.8°F), pulse rateis 118 beats per minute, blood pressure is 84/50 mm Hg, and respiratory rateis 22 breaths per minute. Her mucous membranes are dry. Her heart istachycardic but regular. She has crackles at her right lung base with a scantwheeze. Her abdomen is soft and non tender. The extremities feel cool and herpulses are rapid and thready. The patient is moving all extremities, withoutfocal deficits.What is the most likely diagnosis?
  76. 76. Answer case 5 is SEVER SEPSISSummary: A 73-year-old woman presents from anassisted-living facility withcough, lethargy and hypotension of unknownetiology.Most likely diagnosis: Severe sepsis.Most likely etiology: Pneumonia, nursing-homeacquired`
  77. 77. This woman appears to be sufferingfrom severe sepsis, a clinical entityon the continuum from systemicinflammatory response syndrome toseptic shock with multiorgan systemdysfunction (see below fordefinitions). In her case, the etiology islikely pneumonia, an extremelycommon cause of sepsis in elderlypatients. Sepsis caused by a urinarytract infection (ie, urosepsis) is anotherimportant cause of sepsis in thispopulation.

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