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31 SEPSIS AND SEPTIC SHOCK

31 SEPSIS AND SEPTIC SHOCK
Harrison’s Manual of Medicine

31

SEPSIS AND SEPTIC SHOCK

Definitions
Epidemiology/Etiology/Pathogenesis
Clinical Manifestations
Complications
Diagnosis
Bibliography

Definitions
The systemic inflammatory response syndrome (SIRS), defined in the early 1990s by critical-care specialists, incorporates clinical criteria (fever or hypothermia, tachypnea, tachycardia, and abnormal WBC count) that may be manifestations of microbial infection or conditions of other etiologies. When the syndrome is caused by microbial infection, it is called sepsis. Septic shock refers to the overwhelming of host homeostatic mechanisms by sepsis, which results in hypotension and organ dysfunction. These and related terms are defined in Table 31-1.

Table 31-1 Definitions Used to Describe the Condition of Patients with Sepsis

Epidemiology/Etiology/Pathogenesis
There are 300,000–500,000 cases of sepsis annually in the U.S., and sepsis contributes to >100,000 deaths per year. Approximately two-thirds of cases occur in hospitalized pts. Moreover, ~20–40% of pts with severe sepsis and 40–70% of pts with septic shock have positive blood cultures: 35% of positive cultures yield gram-negative bacteria, ~40% yield gram-positive bacteria, and ~7% yield fungi. Risk factors for gram-negative rod bacteremia include diabetes, lymphoproliferative disease, cirrhosis, burns, invasive procedures or devices, and neutropenia. Risk factors for gram-positive bacteremia include the presence of intravascular catheters or mechanical devices, burns, and IV drug use. The incidence of sepsis appears to be increasing, probably because of an increase in the size of the population with risk factors. Sepsis results from complex host reactions to microbial signal molecules: lipopolysaccharide (LPS, also called endotoxin), peptidoglycan, and lipoteichoic acid of gram-positive bacteria as well as various extracellular enzymes and toxins. The host response is mediated by leukocytes, humoral factors (cytokines, prostaglandins, coagulation factors), and the vascular endothelium.
Clinical Manifestations
Signs of sepsis include the abrupt onset of fever, chills, tachycardia, tachypnea, altered mental status, and/or hypotension, particularly in a pt with localized infection. However, the septic response may develop gradually, and many or all of these signs may be absent. Hyperventilation, disorientation, and confusion are diagnostically useful early signs. Hypotension and DIC may develop. Cutaneous signs are frequent and include cyanosis and ischemic necrosis of peripheral tissue, cellulitis, pustules, bullae, and hemorrhagic lesions. Some skin lesions suggest specific pathogens: petechial or purpuric lesions suggest meningococcemia or Rocky Mountain spotted fever; a bullous lesion surrounded by edema with central hemorrhage and necrosis (ecthyma gangrenosum) suggests Pseudomonas sepsis; generalized erythroderma in a septic pt suggests toxic shock syndrome; bullous lesions in a pt who has eaten raw oysters suggest Vibrio vulnificus sepsis; and the same lesions in a pt after a dog bite suggest Capnocytophaga sepsis. GI manifestations include nausea, vomiting, diarrhea, ileus, gastric ulceration with bleeding, and cholestatic jaundice.
Complications
ARDS (“shock lung”), mediated by pulmonary capillary microvascular injury, develops in ~50% of pts with severe sepsis or septic shock and causes diffuse pulmonary infiltrates and hypoxemia. Sepsis-induced hypotension usually results from a generalized maldistribution of blood flow and blood volume and from hypovolemia due to diffuse capillary leak. After fluid repletion, cardiac output typically increases and systemic vascular resistance falls. Oliguria, azotemia, proteinuria, and nonspecific renal casts are frequent. Renal failure is usually caused by acute tubular necrosis. Thrombocytopenia occurs in 10–30% of cases. Profound thrombocytopenia (60 mmHg and a cardiac index of ³2.2 (L/min)/m2. Higher doses may cause peripheral vasoconstriction with ischemia. Norepinephrine may be used when pts are refractory to dopamine, with dosing carefully titrated to maintain mean blood pressure at >60 mmHg (dose range, 2–20 µg/ min). Ventilatory support is indicated for progressive hypoxemia, hypercapnia, neurologic deterioration, or respiratory muscle failure. Intubation can ensure adequate oxygenation, divert blood flow from the muscles of respiration, prevent aspiration of oropharyngeal contents, and reduce cardiac afterload. Glucocorticoid supplementation (hydrocortisone, 50 mg IV q6h) is indicated only in the rare instance of adrenal insufficiency, which should be suspected in cases of refractory hypotension, fulminant Neisseria meningitidis bacteremia, disseminated tuberculosis, prior glucocorticoid use, or AIDS.

Table 31-2 Initial Antimicrobial Therapy for Severe Sepsis with No Obvious Source in Adults with Normal Renal Function

Despite early diagnosis and prompt and aggressive management, ~20– 35% of pts with severe sepsis and 40–60% of pts with septic shock die within 30 days. Prognosis is affected most by the severity of the pt’s underlying disease and various physiologic parameters. Septic shock is also a strong predictor of short- and long-term mortality. Case-fatality rates are similar for both culture-positive and -negative severe sepsis. Prevention offers the best opportunity to reduce morbidity and mortality from sepsis. Preventive measures include minimizing the number of invasive procedures, limiting the use and duration of indwelling vascular and bladder catheters, reducing the incidence and duration of profound neutropenia, aggressively treating localized infection, and immunizing pts against specific pathogens.

Bibliography

For a more detailed discussion, see Munford RS: Sepsis and Septic Shock, Chap. 124, p. 799, in HPIM-15.

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One comment on “31 SEPSIS AND SEPTIC SHOCK

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