Background
Bacterial sepsis is a clinical term used to describe symptomatic bacteremia, with or without organ dysfunction. Currently, sepsis is commonly defined as the presence of infection in conjunction with the systemic inflammatory response syndrome (SIRS), with severe sepsis understood as sepsis complicated by organ dysfunction and septic shock understood as sepsis-induced acute circulatory failure characterized by persistent arterial hypotension despite adequate volume resuscitation and not explained by other causes.[1]
The term sepsis is often misused and misapplied to patients with fever, leukocytosis, and hypotension due to other causes (pseudosepsis). True sepsis is a common cause of hospitalization in the United States, including in elderly men who are more likely to develop urosepsis as a result of benign urinary tract obstruction caused by prostatic hypertrophy. Patients who have diabetes, systemic lupus erythematosus (SLE), or alcoholism or who are taking steroids are also at increased risk for bacteremia.
Sustained bacteremia, in contrast to transient bacteremia, may result in a sustained febrile response that may be associated with organ dysfunction. The term septicemia refers to the active multiplication of bacteria in the bloodstream that results in an overwhelming infection; the term bloodstream infection (BSI) is also commonly used.
The most important medicolegal concerns regarding sepsis treatment include the following:
- Ensuring that the patient indeed does have sepsis
- Rapidly identifying its source
- Implementing effective treatments
For patient education information, see the Blood and Lymphatic System Center, as well as Sepsis (Blood Infection).
Etiology and Pathophysiology
Sepsis is not a random occurrence and is usually associated with other conditions, such as perforation, compromise, or rupture of an intra-abdominal or pelvic structure.[2] Intrarenal infection (pyelonephritis), renal abscess (intrarenal or extrarenal), acute prostatitis, or prostatic abscess may cause urosepsis in immunocompetent hosts. Urosepsis has also been reported after prostatic biopsy.[3] An abdominal wall abscess shown on an ultrasound is depicted below.
A right lower quadrant abdominal wall abscess and enteric fistula are observed and confirmed by the presence of enteral contrast in the abdominal wall. Sepsis or septic shock may be associated with the direct introduction of microbes into the bloodstream via intravenous (IV) infusion (eg, IV line infections and other device-associated infections). Meningococcemia from a respiratory source may also result in sepsis, with or without associated meningitis.
Bacteremia due to bacteriuria (urosepsis) may complicate cystitis in compromised hosts, and sepsis may be caused by overwhelming pneumococcal infection in patients with impaired or absent splenic function.[4]
The pathophysiology of sepsis is complex and results from the effects of circulating bacterial products, mediated by cytokine release, caused by sustained bacteremia. Cytokines are responsible for the clinically observable effects of the bacteremia in the host.[5, 6, 7, 8] Impaired pulmonary, hepatic, or renal function may result from excessive cytokine release during the septic process.
Prognosis
Sepsis is a common cause of mortality and morbidity worldwide. The prognosis depends on underlying health status and host defenses, prompt and adequate surgical drainage of abscesses, relief of any obstruction of the intestinal or urinary tract, and appropriate and early empiric antimicrobial therapy with the drug spectrum appropriate to the presumed septic source. Thus, early and appropriate empiric antimicrobial therapy and surgical intervention are critical in decreasing mortality and morbidity.
The prognosis in most patients is good, except in those with intra-abdominal or pelvic abscesses due to organ perforation. The underlying physiologic condition of the host is the primary determinant of outcome.
A systematic review by Winters et al suggested that beyond the standard 28-day in-hospital mortality endpoint, ongoing mortality in patients with sepsis remains elevated up to 2 years and beyond.[9] In addition, survivors consistently demonstrate impaired quality of life.[10]
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| Associated With Sepsis (Fever ≥102°F) | Not Associated With Sepsis (Fever ≤102°F) |
| GI tract source Liver Gallbladder Colon Abscess Intestinal obstruction Instrumentation | GI tract source Esophagitis Gastritis Pancreatitis Small bowel disorders GI bleeding |
| GU tract source Pyelonephritis Intra- or perinephric abscess Renal calculi Urinary tract obstruction Acute prostatitis/abscess Renal insufficiency Instrumentation in patients with bacteriuria | GU tract source Urethritis Cystitis Cervicitis Vaginitis Catheter-associated bacteriuria (in otherwise healthy hosts without genitourinary tract disease) |
| Pelvic source Peritonitis Abscess | Upper respiratory tract source Pharyngitis Sinusitis Bronchitis Otitis |
| Lower respiratory tract source Community-acquired pneumonia (with asplenia) Empyema Lung abscess | Lower respiratory tract source Community-acquired pneumonia (in otherwise healthy host) |
| Intravascular source IV line sepsis Infected prosthetic device Acute bacterial endocarditis | Skin/soft-tissue source Osteomyelitis Uncomplicated wound infections |
| Cardiovascular source Acute bacterial endocarditis Myocardial/perivalvular ring abscess | Cardiovascular source Subacute bacterial endocarditis |
| CNS source Bacterial meningitis | |
| CNS = central nervous system; GI = gastrointestinal; GU = genitourinary; IV = intravenous. | |
| Adapted from: Cunha BA, Shea KW. Fever in the intensive care unit. Infect Dis Clin North Am. Mar 1996;10(1):185-209.[18] | |
| Clinical Presentations Mimicking Sepsis | Hemodynamic Parameters Mimicking Sepsis |
| Hemorrhage | Acute pancreatitis |
| Pulmonary embolism | Anaphylaxis |
| Myocardial infarction | Spinal cord injury |
| Pancreatitis | Adrenal insufficiency |
| Diabetic (abdominal crisis) ketoacidosis | |
| Systemic lupus erythematosus flare with abdominal crisis | |
| Ventricular pseudoaneurysm | |
| Massive aspiration/atelectasis | |
| Systemic vasculitis | |
| Diuretic-induced hypovolemia |
| Parameters | Pseudosepsis | Sepsis |
| Microbiologic | No definite source PLUS ≥1 abnormalities Negative blood cultures excluding contaminants | Proper identification/process/source PLUS ≥1 microbiologic abnormalities Positive buffy coat smear result OR 2/3 or 3/3 positive blood cultures |
| Hemodynamic | ⇓ PVR ⇑ CO | ⇓ PVR ⇑ CO Left ventricular dilatation |
| Laboratory | ⇑ WBC count (with left shift) Normal platelet count ⇑ FSP ⇑ Lactate ⇑ D-dimers ⇑ PT/PTT ⇓ Albumin ⇓ Fibrinogen ⇓ Globulins | ⇑ WBC count (with left shift) ⇓ Platelets ⇑ FSP ⇑ Lactate ⇑ D-dimers ⇑ PT/PTT ⇓ Albumin |
| Clinical | ≤102°F ± Tachycardia ± Respiratory alkalosis ± Hypotension | ≥102°F OR Hypothermia ± Mental status changes ± Hypotension |
| CO = cardiac output; FSP = fibrin split products; GI = gastrointestinal; GU = genitourinary; PT/PTT = prothrombin time/partial thromboplastin time; PVR = peripheral vascular resistance; WBC = white blood cell. | ||
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