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Septic shock

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Septic shock with recent SEPSIS-3 definitions.

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Septic shock

  1. 1. SEPTIC SHOCK Dr Kaushal Deep Singh Lecturer, Department of Surgery UPUMS, Saifai
  2. 2. Introduction ■ Earlier Systemic inflammatory response syndrome (SIRS) → sepsis → severe sepsis → septic shock → multiple organ dysfunction syndrome (MODS) → death ■ Now Sepsis → septic shock → organ dysfunction/multiple organ dysfunction syndrome (MODS) → multiple organ failure syndrome → death ■ SIRS is defined as 2 or more of the following variables – Fever of more than 38°C (100.4°F) or less than 36°C (96.8°F) – Heart rate of more than 90 beats per minute – Respiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO 2) of less than 32 mm Hg – Abnormal white blood cell count (>12,000/µL or < 4,000/µL or >10% immature [band] forms)
  3. 3. ■ New 2016 definition, also called Sepsis-3, eliminates the requirement for the presence of systemic inflammatory response syndrome (SIRS) to define sepsis, and it removed the severe sepsis definition. What was previously called severe sepsis is now the new definition of sepsis. ■ Sepsis is defined as life-threatening organ dysfunction due to dysregulated host response to infection. ■ Bacteremia is defined as the presence of viable bacteria within the liquid component of blood. – May be primary (without an identifiable focus of infection) or, more often, secondary (with an intravascular or extravascular focus of infection). – Although sepsis is associated with bacterial infection, bacteremia is not a necessary ingredient in the activation of the inflammatory response that results in severe sepsis. – Septic shock is associated with culture-positive bacteremia in only 30-50% of cases.
  4. 4. ■ Septic Shock is defined by persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mm Hg or higher; and a serum lactate level greater than 2 mmol/L (18 mg/dL) despite adequate volume resuscitation. ■ Organ Dysfunction is defined as an acute change in total Sequential Organ Failure Assessment (SOFA) score greater than 2 points secondary to the infectious cause. ■ For screening purposes, a shorter version of the SOFA score, termed quick SOFA (qSOFA), demonstrated to have reasonable accuracy in the settings outside the ICU. ■ qSOFA is defined by two or more of a total of the following three components: – altered mental status, – respiratory rate of 22 or higher, and
  5. 5. ■ Multiple organ dysfunction syndrome (MODS) is defined as the presence of altered organ function in a patient who is acutely ill and in whom homeostasis cannot be maintained without intervention. ■ MODS may eventually lead to multiple organ failure syndrome (MOFS) and death. ■ Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common manifestations of MODS or MOFS. ■ However, other conditions besides sepsis can cause MODS, including trauma, burns, and severe hemorrhagic shock.
  6. 6. ■ Acute lung injury and acute respiratory distress syndrome : Berlin Definition of ARDS classifies ARDS as mild, moderate, or severe : – Mild ARDS – An oxygenation abnormality with a PaO2/FIO2 ratio of 200-300 and a positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) of 5 cm H2O or higher – Moderate ARDS – A PaO2/FIO2 ratio of 100-200 and a PEEP of 5 cm H2O or higher – Severe ARDS – A PaO2/FIO2 ratio of 100 or less and a PEEP of 5 cm H2O or higher – Bilateral opacities on chest radiographs that are not fully explained by effusions, lobar/lung collapse, or nodules – Edema not of cardiac origin or caused by fluid overload – In the absence of risk factors for ARDS, this requires objective assessment (eg, via echocardiography) – Occurrence within 1 week of a known clinical insult or worsening respiratory symptoms
  7. 7. ■ MODS staging : Two well-defined forms of MODS exist. 1. In the more common form of MODS, the lungs are the predominant, and often the only, organ system affected until very late in the disease. – Present with a primary pulmonary disorder (eg, pneumonia, aspiration, lung contusion, near- drowning, chronic obstructive pulmonary disease [COPD] exacerbation, hemorrhage, or pulmonary embolism [PE]). – Pulmonary dysfunction may be accompanied by encephalopathy or mild coagulopathy and persists for 2-3 weeks. At this time, the patient either begins to recover or progresses to develop fulminant dysfunction in other organ systems. – Patients who develop another major organ dysfunction often do not survive. 2. In the second, less common, form of MODS, the presentation is quite different. – Inciting source of sepsis in organs other than the lung; the most common sources are intra- abdominal sepsis, extensive blood loss, pancreatitis, and vascular catastrophes. – Not only does ARDS develop early, but dysfunction also develops in other organ systems, including the hepatic, hematologic, cardiovascular, and renal systems and central nervous system (CNS). – Patients remain in a pattern of compensated dysfunction for several weeks, then either recover or deteriorate further.
  8. 8. Pathophysiology
  9. 9. Causative microorganisms ■ Before the introduction of antibiotics, gram-positive bacteria were the principal organisms that caused sepsis. ■ Subsequently, gram-negative bacteria became the key pathogens causing severe sepsis and septic shock. ■ Currently, however, the rates of severe sepsis and septic shock due to gram-positive organisms are rising again because of the more frequent use of invasive procedures and lines in critically ill patients. ■ As a result, gram-positive and gram-negative microorganisms are now about equally likely to be causative pathogens in septic shock. ■ Respiratory tract and abdominal infections are the most frequent causes of sepsis, followed by urinary tract and soft-tissue infections. ■ Lower respiratory tract infections cause septic shock in 35-50% of patients. The following are the common pathogens: – Streptococcus pneumoniae – Klebsiella pneumoniae – Escherichia coli – Legionella spp – Haemophilus spp – Staphylococcus aureus
  10. 10. ■ Abdominal and GI tract infections cause septic shock in 20-40% of patients. The following are the common pathogens: – E coli – Enterococcus spp – Bacteroides fragilis – Acinetobacter spp – Pseudomonas spp – Enterobacter spp – Salmonella spp – Klebsiella spp – Anaerobes ■ Urinary tract infections cause septic shock in 10-30% of patients. The following are the common pathogens: – E coli – Proteus spp – Klebsiella spp – Pseudomonas spp
  11. 11. ■ Infections of the male and female reproductive systems cause septic shock in 1- 5% of patients. The following are the common pathogens: – Neisseria gonorrhoeae – Gram-negative bacteria – Streptococci – Anaerobes ■ Soft-tissue infections cause septic shock in 5-10% of patients. The following are the common pathogens: – S aureus – Staphylococcus epidermidis – Streptococci – Clostridium spp ■ Infections due to foreign bodies cause septic shock in 1-5% of patients. S aureus, S epidermidis, and fungi (eg, Candida species) are the common pathogens. ■ Miscellaneous infections, such as CNS infections, also cause septic shock in 1-5% of patients. Neisseria meningitidis is a common cause of such infections.
  12. 12. A 72-year-old woman comes to you 52 hours following uncomplicated laparoscopic cholecystectomy for gallstone disease. She was found unconscious on the ward with generalized tonic-clonic seizures, requiring 20 mg diazepam. Her sodium level is 112 mmol/L. During surgery she received 3 L of 5% dextrose with 20 mmol/L potassium chloride. Her potassium and urea and creatinine are within normal limits. There are no signs of heart failure. Her plasma osmolality is 265 mOsm/kg and her urinary osmolality is 566 mOsm/kg. Which of the following is the most likely cause for her low sodium? A. Excess 5% dextrose B. Addison's disease C. Syndrome of inappropriate antidiuretic hormone secretion D. Nephrotic syndrome E. Congestive cardiac failure
  13. 13. Risk factors ■ Extremes of age (< 10 years and >70 years) ■ Primary diseases (eg, liver cirrhosis, alcoholism, diabetes mellitus, cardiopulmonary diseases, solid malignancy, and hematologic malignancy) ■ Immunosuppression (eg, from neutropenia, immunosuppressive therapy [eg, in organ and bone marrow transplant recipients], corticosteroid therapy, injection or IV drug use, complement deficiencies, asplenia) ■ Major surgery, trauma, burns ■ Invasive procedures (eg, placement of catheters, intravascular devices, prosthetic devices, hemodialysis and peritoneal dialysis catheters, or endotracheal tubes) ■ Previous antibiotic treatment ■ Prolonged hospitalization ■ Underlying genetic susceptibility ■ Other factors (eg, childbirth, abortion, and malnutrition)
  14. 14. Signs and symptoms ■ Signs and symptoms of sepsis are often nonspecific and include the following : – Fever, chills, or rigors – Confusion – Anxiety – Difficulty breathing – Fatigue, malaise – Nausea and vomiting ■ Typical symptoms of systemic inflammation may be absent in severe sepsis, especially in elderly individuals. ■ Identify any potential source of infection.
  15. 15. Laboratory tests ■ Complete blood count with differential count – WBC count higher than 15,000/µL or a neutrophil band count higher than 1500/µL has about a 50% correlation with bacterial infection. – WBC counts higher than 50,000/µL or lower than 300/µL are associated with significantly decreased survival rates. – Hemoglobin concentration dictates oxygen-carrying capacity in blood, keeping the hemoglobin concentration above 7 g/dL is usually practiced. – Platelet count will fall with persistent sepsis, and disseminated intravascular coagulation (DIC) may develop. ■ Coagulation studies (eg, prothrombin time [PT], activated partial thromboplastin time [aPTT], fibrinogen levels) – PT and the aPTT are elevated in DIC, fibrinogen levels are decreased, and fibrin split products are increased.
  16. 16. ■ Blood chemistry (eg, sodium, chloride, magnesium, calcium, phosphate, glucose, lactate) – Sodium and chloride levels are abnormal in severe dehydration. – Decreased bicarbonate can point to acute acidosis - sodium bicarbonate therapy is not recommended to improve hemodynamics or replace vasopressor requirements in patients with metabolic acidemia from hypoperfusion whose pH level is 7.15 or greater. – Hyperglycemia is associated with higher mortality. – Serum lactate is perhaps the best serum marker for tissue perfusion. Lactate levels > 2.5 mmol/L are associated with an increase in mortality. Lactate levels higher than 4 mmol/L in patients with suspected infection have been shown to yield a 5-fold increase in the risk of death and are associated with a mortality approaching 30%. ■ Renal and hepatic function tests (eg, creatinine, blood urea nitrogen, bilirubin, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, albumin, lipase)
  17. 17. ■ American College of Critical Care Medicine (ACCCM) does not recommend the routine use of free cortisol measurements in critically ill patients. ■ Blood cultures (Surviving Sepsis Campaign recommends obtaining at least 2 blood cultures before antibiotics are administered, with 1 percutaneously drawn and the other(s) obtained through each vascular access) - blood cultures are positive in fewer than 50% of cases of sepsis. ■ Urinalysis and urine cultures - Urinary tract infection (UTI) is a common source for sepsis, especially in elderly individuals. Adults who are febrile without localizing symptoms or signs have a 10-15% incidence of occult UTI. ■ Gram stain and culture of secretions and tissue
  18. 18. Imaging studies ■ Chest, abdominal, or extremity radiography – Most patients who present with sepsis have pneumonia. – Chest radiography detects infiltrates in about 5% of febrile adults without localizing signs of infection. – Chest radiography is useful in detecting radiographic evidence of ARDS - bilateral hazy, symmetric homogeneous opacities, which may demonstrate air bronchograms, ground- glass opacities. – Supine and upright or lateral decubitus abdominal radiographs - bowel obstruction or perforation – Osteomyelitis, necrotizing fasciitis, gas gasgrene ■ Abdominal ultrasonography – acute cholecystitis or ascending cholangitis, acute pancreatitis ■ Computed tomography of the abdomen or head – intra-abdominal abscess or a retroperitoneal source of infection, meningitis (Lumbar Puncture)
  19. 19. Management ■ Admission to the hospital – responders (general ward); non-responders (ICU) ■ Cardiac monitoring, noninvasive blood pressure monitoring, and pulse oximetry. ■ Goal-directed therapy VS direct and aggressive individualized care [United States (ProCESS [Protocolized Care for Early Septic Shock]), Australia (ARISE [Australasian Resuscitation In Sepsis Evaluation]), and the United Kingdom (ProMISe [Protocolised Management In Sepsis]). ■ Measuring lactate, targeting ScvO2 values, and insertion of a central venous catheter were not associated with improved outcomes. What was important was the direct and aggressive individualized care each patient received, including early bacteriologic cultures of appropriate sites (eg, blood, urine, sputum), early and correct institution of broad-spectrum antibiotics, restoration of blood pressure, and reversal of evidence of end-organ perfusion.
  20. 20. Management (contd…) ■ Management principles for septic shock include the following: – Early recognition – Early and adequate antibiotic therapy – Source control – Early hemodynamic resuscitation and continued support – Proper ventilator management with low tidal volume in patients with acute respiratory distress syndrome (ARDS) ■ Treatment of patients with septic shock has the following major goals: – Start adequate antibiotics (proper spectrum and dose) as early as possible – Resuscitate the patient from septic shock by using supportive measures to correct hypoxia, hypotension, and impaired tissue oxygenation (hypoperfusion) – Identify the source of infection and treat with antimicrobial therapy, surgery, or both (source control) – Maintain adequate organ system function, guided by cardiovascular monitoring, and interrupt the
  21. 21. ■ First 6 hours of resuscitation of a critically ill patient with sepsis or septic shock are critical. The following should be completed within 3 hours: – Obtain the lactate level – Obtain blood cultures before administering antibiotics – Administer broad-spectrum antibiotics – Administer 30 mL/kg of crystalloid solution for hypotension or for lactate levels of 4 mmol/L or higher ■ Following should be completed within 6 hours: – Administer vasopressors for hypotension that does not respond to initial fluid resuscitation to maintain a mean arterial pressure (MAP) of 65 mm Hg or higher – If hypotension persists despite volume resuscitation or the initial lactate level is 4 mmol/L or higher, then measure central venous pressure (CVP) (aiming for ≥8 mm Hg), measure central venous oxygen saturation (ScvO 2) (aiming for ≥70%), and normalize lactate levels
  22. 22. Steps in Management 1. Venous access 2. Urinary catheterization 3. Respiratory support 4. Intubation and mechanical ventilation 5. Circulatory support 6. Correction of anemia and coagulopathy 7. Antimicrobial therapy 8. Temperature control 9. Metabolic and nutritional support
  23. 23. Pharmacotherapy ■ Alpha-/beta-adrenergic agonists (eg, norepinephrine, dopamine, dobutamine, epinephrine, vasopressin, phenylephrine) ■ Isotonic crystalloids (eg, normal saline, lactated Ringer solution) ■ Volume expanders (eg, albumin) ■ Antibiotics (eg, cefotaxime, ticarcillin-clavulanate, piperacillin- tazobactam, imipenem-cilastatin, meropenem, clindamycin, metronidazole, ceftriaxone, ciprofloxacin, cefepime, levofloxacin, vancomycin) ■ Corticosteroids (eg, hydrocortisone, dexamethasone)
  24. 24. Surgery ■ Certain conditions will not respond to standard treatment for septic shock until the source of infection is surgically removed - – Intra-abdominal sepsis [perforation, abscesses] – Empyema – Mediastinitis – Cholangitis – pancreatic abscesses – pyelonephritis or renal abscess from ureteric obstruction – infective endocarditis – septic arthritis – infected prosthetic devices – deep cutaneous or perirectal abscess – necrotizing fasciitis
  25. 25. ■ Urgent management is indicated for hemodynamically stable patients without evidence of acute organ failure, delay of invasive procedures for as long as 24 hours may be possible if the patient receives very close clinical monitoring and appropriate antimicrobial therapy. ■ When possible, percutaneous drainage of abscesses and other well- localized fluid collections is preferred to surgical drainage. ■ However, any deep abscess or suspected necrotizing fasciitis should undergo drainage in the surgical suite.

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