Goutham seminar


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Goutham seminar

  2. 2.  In 1914, Schottmueller wrote, “Septicemia is a state of microbial invasion from a portal of entry into the blood stream which causes sign of illness.”
  3. 3.  Infection A microbial phenomenon characterized by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms. Bacteremia The presence of viable bacteria in the blood. SIRS systemic level of acute inflammation, that may or may not be due to infection, and is generally manifested as a combination of vital sign abnormalities. Severe SIRS SIRS in which at least 1 major organ system has failed
  4. 4.  Sepsis SIRS which is secondary to infection. Severe sepsis Severe SIRS which is secondary to infection. Shock It is a serious, life threatening medical condition characterized by a decrease in tissue perfusion to a point that is inadequate to meet cellular metabolic needs. Septic shock sepsis with hypotension(arterial bp<90mm hg systolic) for 1 hr despite adequate fluid resuscitation.( Or ).need for vassopressors to maintain systolic bp>=90mm or mean arterial pressure >=70mmhg. Multiple Organ Dysfunction Syndrome (MODS) The presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.
  5. 5.  Requires 2 of the following 4 features to be present: o Temp >38° or <36.0° C o Tachypnea RR>20 o Tachycardia (HR>90, in the absence of intrinsic heart disease) o WBC > 12,000/mm3 or <4,000/mm3 or >10% band forms on differential
  6. 6.  Must meet criteria for SIRS, plus 1 of the following: o Altered mental status o SBP<90mmHg or fall of >40mmHg from baseline o Impaired gas exchange (PaO2/FiO2 ratio<200-250) o Metabolic acidosis (pH<7.30 & lactate > 1.5 x upper limit of normal) o Oliguria (<0.5mL/kg/hr) or renal failure o Hyperbilirubinemia o Coagulopathy o platelets < 80,000-100,000/mm3, o INR >2.0, PTT >1.5 x control, o elevated fibrin degredation products
  7. 7. Altered Tachycardia Consciousness Hypotensio Confusion n Psychosis  CVP  PAOP Tachypnea PaO2 <70 mm Oliguria Hg Anuria SaO2 <90%  CreatininePaO2/FiO2 300  Platelets Jaundice  PT/APTT  Enzymes  Protein C  Albumin  D-dimer  PT
  9. 9.  It is not precisely understood, but it involves a complex interaction between the pathogen and the hosts immune system. Physiological response to localized infection: o Influx of activated PMN leukocytes & monocytes  release of inflammatory mediators o Local vasodilatation & increased endothelial permeability o Activation of the coagulation cascade. The same occurs in septic shock but at a systemic level.  Diffuse endothelial disruption  Increased vascular permeability  Vasodilatation  Thrombosis of end organ capillaries
  10. 10. Infection Inflammatory Endothelial Vasodilation Mediators DysfunctionHypotension Microvascular Plugging Vasoconstriction Edema Maldistribution of Microvascular Blood Flow Ischemia Cell Death Organ Dysfunction
  11. 11. 1. Extremes of age2. Indwelling lines/catheters3. Immunocompromised states4. Malnutrition5. Alcoholism6. Malignancy7. Diabetes8. Cirrhosis9. Male sex10. Genetic predisposition?
  12. 12. Recognition of Septic Shock: Inflammatory triad-  Fever  Tachycardia Warm  flushed skin Hypoperfusion shock  Altered sensorium  Urine output  Wide pulse pressure.......bounding pulses
  13. 13.  Hypotension  Cold and clammy skin  Mottling  Tachycardia Cold shock  Cyanosis  Narrow pulse pressure  Hypoxemia  Acidosis.
  14. 14.  Localizing symptoms that are most useful clues to the etiology sepsis:  Head and neck infections - Severe headache, neck stiffness, altered mental status, earache, sore throat, sinus pain or tenderness, cervical or submandibular lymphadenopathy Chest and pulmonary infections - Cough (especially if productive), pleuritic chest pain, dyspnea.(Streptococcus pneumoniae,Klebsiella pneumoniae,Staphylococcus aureus) Abdominal and GI infections - Abdominal pain, nausea, vomiting, diarrhea(E coli,Acinetobacter species,Enterobacter species,Salmonella species) Pelvic and genitourinary infections - Pelvic or flank pain, vaginal or urethral discharge, dysuria, frequency, urgency(E coli,Proteus species,Klebsiella species) Bone and soft-tissue infections - Focal pain or tenderness, focal erythema, edema, fluctuance(S aureus,Staphylococcus epidermidis,Streptococci)
  15. 15.  Laboratory studies o CBC o Comprehensive chemistry panel o Coagulation studies o Blood & urine cultures Imaging studies o Chest radiography o Abdominal radiography o Others according to the suspected cause.
  16. 16.  CBC: o The WBC count and differential. o Hemoglobin concentration dictates oxygen-carrying capacity in blood. o The goal is to maintain hematocrit >30% and hemoglobin >10 g/dL. o Platelets are an acute-phase reactant and are typically elevated in the setting of inflammation. However, platelet counts may decrease in the setting of DIC.
  17. 17.  Sodium and chloride levels are abnormal in severe dehydration.  Decreased bicarbonate can point to acute acidosis.  Increased BUN and creatinine levels can point to severe dehydration or renal failure.  Glucose control is important in the management of sepsis, with hyperglycemia associated with higher mortality.• LFTs and bilirubin, alkaline phosphatase, and lipase levels are important in evaluating multiorgan dysfunction or a potential source (eg, biliary disease, pancreatitis, hepatitis).
  18. 18.  It is the best serum marker for tissue perfusion. There is also evidence that lactate can be elevated in sepsis in the absence of tissue hypoxia due to mitochondrial dysfunction and down-regulation of pyruvate dehydrogenase, which is the first step in oxidative phosphorylation. Lactate levels >2.5 mmol/L are associated with an increase in mortality. It has been hypothesized that lactate clearance is a measure of tissue reperfusion and an indication of adequate therapy.
  19. 19.  Coagulation studies (PT/aPTT) o PT and activated aPTT are elevated in DIC. o Fibrinogen levels are decreased and FDP are increased in the setting of DIC. Blood cultures o Blood cultures should be obtained in patients who have suspected sepsis in order to isolate a specific organism and tailor antibiotic therapy. o Positive in < 50% of cases of sepsis. o A set of cultures from an indwelling intravenous catheter is especially important, as these catheters are a frequent source of bacteremia. Urinalysis and urine culture o Urinary tract infection is a common source of sepsis, especially in elderly patients. o Febrile adults without localizing symptoms or signs have a rate of occult urinary tract infection of 10-15%. Gram stain and culture, when applicable o Sputum specimen should be obtained if pneumonia is suspected. o Any abscess should be drained promptly, and purulent material sent to the microbiology laboratory for analysis. o CSF specimen should be obtained if meningitis is suspected.
  20. 20. • CXR  routine in the workup of fever with an unclear etiology. o Infiltrates are detected with a chest radiograph in about 5% of febrile adults without localizing signs of infection.  Abdominal plain films should be obtained if clinical evidence of bowel obstruction or perforation exists.  Abdominal ultrasonography is indicated when evidence of acute cholecystitis or ascending cholangitis exists
  21. 21. The initial treatment of sepsisand septic shock involves the administration of supplemental oxygen andvolume infusion with isotonic crystalloids
  22. 22.  Broad spectrum antibiotics Abscess should be drained, necrotic tissue excised Blood glucose levels normalized Replacement-dose corticosteroids
  23. 23.  Patients with septic shock should be treated in an ICU. Apache score The following should be monitored frequently: o systemic pressure o CVP o pulse oximetry o ABGs o blood glucose o lactate, and electrolyte levels o renal function o Urine output, a good indicator of renal perfusion, should be measured, usually with an indwelling catheter
  24. 24. An initial assessment of airway and breathing is very important in a patient with septic shock.Supplemental oxygen should be administered to all patients with suspected sepsis.
  25. 25.  Patients with suspected septic shock require an initial crystalloid fluid challenge of 20-30 mL/kg (1-2 L) over a period of 30-60 minutes with additional fluid challenges at rates of up to 1 L over 30 minutes. Crystalloid administration is titrated to a CVP goal between 8 and 12 mm Hg or signs of volume overload (dyspnea, pulmonary rales, or pulmonary edema on the chest radiograph). A fluid challenge refers to the rapid administration of volume over a particular time period followed by an assessment of the response. Patients with septic shock often require a total 4-6 L or more of crystalloid resuscitation. It is also important to monitor urine output (UOP) as a measure of dehydration. UOP <30-50 mL/h should prompt further fluid resuscitation
  26. 26.  Vasopressor administration is required for persistent hypotension once adequate intravascular volume expansion has been achieved. Persistent hypotension is typically defined as systolic blood pressure (SPB) <90 mm Hg or mean arterial pressure (MAP) <65 mm Hg with altered tissue perfusion. The goal of vasopressor therapy is to reverse pathologic vasodilation and altered blood flow distribution. The recommended first-line agent for septic shock is either norepinephrine or dopamine
  27. 27.  Norepinephrine:  Has predominant alpha-receptor agonist effects results in potent peripheral arterial vasoconstriction without significantly increasing heart rate or cardiac output.  So it is preferred in warm septic shock where peripheral vasodilatation exists in association with normal or increased cardiac output.  Dose: 5-20 mcg/min Dopamine:  has a much greater effect on beta-receptors  increasing mean arterial pressure primarily through increasing myocardial contractility, stroke volume, and heart rate.  At high doses it has some alpha-receptor effect and so causing peripheral vasoconstriction.  It is more useful in the setting of cold shock, where peripheral vasoconstriction exists and cardiac output is too low to maintain tissue perfusion.  Doses range from 2-20 mcg/kg/min.
  28. 28.  Antibiotics should be administered within the first hour of recognition of septic shock, and delays in antibiotic administration have been associated with increased mortality. Selection of particular antibiotic agents is empirically based on  an assessment of the patients underlying host defenses,  the potential source of infection, and  the most likely responsible organisms. Antibiotic choice must be broad spectrum, covering gram- positive, gram-negative, and anaerobic bacteria when the source is unknown.
  29. 29. Clinical condition Antibiotics regimens(intravenous therapy)Immunocompetent adult Ceftriaxone(2g q24h) or piperacillin- tazobactum(3.375g q4-6h)or meropenem(1g q8h) or(cefepime 2g q12h)AIDS piperacillin-tazobactum(3.375g q4-6h)or meropenem(1g q8h) or(cefepime 2g q12h)
  30. 30.  One regimen for septic shock of unknown cause is Ceftriaxone(2g q24h) or piperacillin- tazobactum(3.375g q4-6h)or meropenem(1g q8h) or(cefepime 2g q12h) Vancomycin must be added if resistant staphylococci or enterococci are suspected. If there is an abdominal source, a drug effective against anaerobes should be included “metronidazole” Antibiotics are continued for at least 5 days after shock resolves and evidence of infection subsides Abscesses must be drained and necrotic tissues (eg, infarcted bowel, gangrenous gallbladder, abscessed uterus) surgically excised.
  31. 31.  It has theoretical benefits in the setting of severe sepsis by inhibiting the massive inflammatory cascade. Recent guidline is that steroids should be administered only in patients with septic shock whose hypotension is poorly responsive to fluid resuscitation and vasopressor therapy. Hydrocortisone 200–300 mg/day, for 7 days in three or four divided doses or continuos infusion.
  32. 32.  Recombinant drug with fibrinolytic and anti-inflammatory activity, seems beneficial for severe sepsis and septic shock if begun early; benefit has been shown only in patients with significant risk of death. Dose: 24 mcg/kg/h by continuous IV infusion for 96 h. Bleeding is the most common complication; Contraindications include:  hemorrhagic stroke within 3 mo,  spinal or intracranial surgery within 2 mo,  acute trauma with a risk of bleeding  intracranial neoplasm.
  33. 33.  Normalization of blood glucose improves outcome in critically ill patients, even those not known to be diabetic. A continuous IV insulin infusion (crystalline zinc 1 to 4 U/h) is titrated to maintain glucose between 80 to 110 mg/dL . This approach necessitates frequent (eg, q 1 to 4 h) glucose measurement.
  34. 34.  Intermittent haemodialysis and continuous veno venous haemofiltration (CVVH) are considered equivalent. CVVH offers easier management in haemodynamically unstable patients.
  35. 35.  Use either low-dose unfractionated heparin or low-molecular weight heparin. Use a mechanical prophylactic device, such as compression stockings or an intermittent compression device, when heparin is contraindicated. Use a combination of pharmacologic and mechanical therapy for patients who are at very high risk for DVT.
  36. 36.  Discuss advance care planning with patients and families. Describe likely outcomes and set realistic expectations.
  37. 37.  As sepsis progresses to septic shock,the risk of dying increases substantially. Sepsis is usually reversible whereas patients with septic shock often succumb despite aggressive therapy. So prevention offers the best oppurtunity to reduce mortality and morbidity.
  38. 38.  Special consideration must be given to neonates, infants, and small children with regard to fluid resuscitation, appropriate antibiotic coverage, intravenous (IV) access, and vasopressor therapy.