Critical Care Medicine 978-1-4963-0291-5 chapter 27

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CHAPTER 27 • Sepsis and Septic Shock

Table 27-1.  Sepsis Syndrome Criteria I. Clinical evidence of infection (required) II. Major criteria (two of four required) Fever or hypothermia (temperature >100.4°F or <96°F) Tachypnea or high minute ventilation (respiratory rate >20 or minute ventilation >10 L)

Tachycardia (pulse >90 in the absence of intrinsic heart disease or drug therapy inhibiting tachycardia) Leukocytosis or leukopenia (WBC >10,000/mm 3 or <4,000/mm 3 ) or greater than 10% band forms on differential III. Acute impairment of organ system function (one required) Altered mental status (reduction in Glasgow coma score >2 points) Hypotension (SBP < 90 mm Hg or fall in BP > 40 mm Hg refractory to fluid challenge) Impaired gas exchange or acute respiratory distress syndrome (PaO 2 /FiO 2 ratio <300) Metabolic acidosis/lactic acidosis Oliguria or renal failure (urine output <0.5 mL/kg/h) Hyperbilirubinemia Coagulopathy (platelet count <80,000/mm 3 or a 50% decline within 48 hours; INR > 2.0; PTT > 1.5 × control with elevated fibrin degradation products)

Common examples include growth of skin flora in one of several blood culture bottles, the recovery of a light growth of Staphylococcus aureus from sputum of a ventilated patient, or demonstration of a few colonies of Candida albicans in the urine of a patient with an indwelling urinary catheter. Perhaps the most convincing evidence of infection comes when several blood cultures obtained at the onset of the episode grow an identical pathogen consistent with the patient’s clinical situation, for example, recovery of Escherichia coli in multiple blood cultures from an elderly man with bladder outlet obstruction and pyuria. Unfortunately, positive blood cultures are recovered in the minority of patients with advanced sepsis, and blood cultures are seldom positive if obtained after antimicrobial therapy is started. Despite historical teaching, there is little prognostic import of having positive blood cultures, unless bac- teremia cannot be eradicated. Inability to clear the circulation of organisms is often associated with an unresolved focus of infection (e.g., endocarditis or an infected foreign object) and portends a worse prognosis. Remarkably, host responses that mimic sepsis are encountered in noninfected patients with severe pancreatitis, trauma, or burns, as these conditions produce similar biochemical changes, disordered physiology, clinical presentation, and outcome. This observation suggests that infection is not essen- tial but rather that microbiologic stimulation acts merely as one disease trigger. The lung is the most common site of infection leading to life-threatening sepsis, accounting for

roughly half of all cases. Intra-abdominal infections (20% to 25%) and urinary tract infections (approx. 10%) are the next most common, with all other sites comprising the remaining 15% of infections. MICROBIOLOGY Bacteria, fungi, parasites, and viruses all can incite the sepsis syndrome. Because of the relatively high incidence of bacterial infections and relative ease in recovery of these organisms, bacteria are most com- monly implicated. Limitations of diagnostic tech- niques make causative viruses difficult to identify. Historically, fungal infections were rarely etiologic in immunocompetent hosts, but with improved antibacterial agents and support techniques, increased numbers of immunocompetent patients now survive long enough to acquire a fungal infec- tion. Distressingly, the frequency of fungal, particu- larly Candida infection, has risen dramatically over the past decades and now accounts for almost 10% of all sepsis-related episodes. When a bacterial pathogen is identified, the fre- quency of gram-positive versus gram-negative bac- teria is roughly 50:50. Discussions of the likelihood of gram-positive versus gram-negative infection are of limited value; the prevalence of organisms varies by location and over time, “cycling” under antibiotic pressure. Furthermore, knowing the frequency of each type of bacteria across a population is not partic- ularly helpful in designing the initial treatment plan for an individual patient, except that such informa- tion can highlight unusual local resistance patterns.

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