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Goutham seminar

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  • 1. Dr. VENKAT NARAYANA GOUTHAM.V
  • 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.  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.  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.  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.  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. 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
  • 8. BACTEREMIA TRAUMAINFECTION SEPSIS SEPSIS SIRS BURNS PANCREATITIS
  • 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. Infection Inflammatory Endothelial Vasodilation Mediators DysfunctionHypotension Microvascular Plugging Vasoconstriction Edema Maldistribution of Microvascular Blood Flow Ischemia Cell Death Organ Dysfunction
  • 11. 1. Extremes of age2. Indwelling lines/catheters3. Immunocompromised states4. Malnutrition5. Alcoholism6. Malignancy7. Diabetes8. Cirrhosis9. Male sex10. Genetic predisposition?
  • 12. Recognition of Septic Shock: Inflammatory triad-  Fever  Tachycardia Warm  flushed skin Hypoperfusion shock  Altered sensorium  Urine output  Wide pulse pressure.......bounding pulses
  • 13.  Hypotension  Cold and clammy skin  Mottling  Tachycardia Cold shock  Cyanosis  Narrow pulse pressure  Hypoxemia  Acidosis.
  • 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.  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.  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.  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.  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.  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. • 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. The initial treatment of sepsisand septic shock involves the administration of supplemental oxygen andvolume infusion with isotonic crystalloids
  • 22.  Broad spectrum antibiotics Abscess should be drained, necrotic tissue excised Blood glucose levels normalized Replacement-dose corticosteroids
  • 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. 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.  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.  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.  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.  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. 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.  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.  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.  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.  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.  Intermittent haemodialysis and continuous veno venous haemofiltration (CVVH) are considered equivalent. CVVH offers easier management in haemodynamically unstable patients.
  • 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.  Discuss advance care planning with patients and families. Describe likely outcomes and set realistic expectations.
  • 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.  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.

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