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Bacterial Sepsis

  • Author: Burke A Cunha, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Mar 18, 2016
 

Practice Essentials

Bacterial sepsis refers to symptomatic bacteremia, with or without organ dysfunction. Sepsis is commonly defined as the presence of infection in conjunction with the systemic inflammatory response syndrome (SIRS); severe sepsis, as sepsis complicated by organ dysfunction; and septic shock, as a subset of sepsis in which underlying circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than sepsis alone (identified using the clinical criteria of hypotension requiring vasopressor therapy to maintain mean blood pressure of 65 mm Hg or greater and having a serum lactate level >2 mmol/L after adequate fluid resuscitation[3] ).

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.[1] 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.[2] An abdominal wall abscess is present on the CT scan shown below.

A right lower quadrant abdominal wall abscess and A right lower quadrant abdominal wall abscess and enteric fistula are observed and confirmed by the presence of enteral contrast in the abdominal wall.

Signs and symptoms

The history and physical examination may suggest the likely source of the septic process and thereby help determine the appropriate antimicrobial therapy. General signs and symptoms may include the following:

  • Fever, with or without shaking chills
  • Impaired mental status (in the setting of fever or hypoperfusion)
  • Increased breathing rate resulting in respiratory alkalosis
  • Warm or cold skin, depending on the adequacy of organ perfusion and dilatation of the superficial vessels of the skin

The following factors suggest an IV line infection:

  • An infected central line site; peripheral venous lines are almost never involved, and arterial lines are rarely associated with bacteremia
  • Elimination of other potential sources, in conjunction with long-term IV line placement

The following factors suggest a gastrointestinal (GI) or genitourinary (GU) infection:

  • History of antecedent conditions predisposing to perforation or abscess
  • Abdominal pain – Diffuse pain (suggesting pancreatitis or generalized peritonitis), right upper quadrant (RUQ) tenderness (gallbladder etiology), right lower quadrant (RLQ) tenderness (appendicitis or Crohn disease), or discrete left lower quadrant (LLQ) tenderness (diverticulitis)
  • Abnormalities on rectal examination – Exquisite tenderness (suggesting a prostatic abscess) or an enlarged noninflamed prostate (benign prostatic hyperplasia)
  • Pertinent GU findings – Antecedent history of pyelonephritis, stone disease, congenital abnormal collecting system, prostate enlargement, or prostatic or renal operations or procedures; costovertebral angle tenderness (suggesting pyelonephritis)

Special considerations include the following:

  • Elderly patients may present with peritonitis and may not experience rebound tenderness of the abdomen
  • An acute surgical abdomen in a pregnant patient may be difficult to diagnose; the most common cause of sepsis in pregnancy is urosepsis due to an obstructed urinary tract

Sepsis is usually associated with other conditions, such as the following:

  • GI tract – Liver disease, gallbladder disease, colon disease, abscess, intestinal obstruction, and GI instrumentation
  • GU tract – Pyelonephritis, intra- or perinephric abscess, renal calculi, urinary tract obstruction, acute prostatitis or abscess, renal insufficiency, and GU instrumentation
  • Pelvis – Peritonitis and pelvic abscess
  • Lower respiratory tract – Community-acquired pneumonia (with asplenia), empyema, and lung abscess
  • Vascular system – Infected IV line or prosthetic device
  • Heart and cardiac vasculature – Acute bacterial endocarditis and myocardial or perivalvular ring abscess

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies that may be considered include the following:

  • Complete blood (CBC) count – May show elevated or low white blood cell count, anemia, and/or thrombocytopenia
  • Bacterial cultures – Blood cultures at admission; culture of the catheter tip (for suspected central IV line sepsis); urine culture if urinary tract source is suspected
  • Stained buffy coat smears or Gram staining of peripheral blood (may be helpful in certain infections)
  • Urine studies (Gram stain, urinalysis, and urine culture)
  • Certain biomarkers, such as procalcitonin and presepsin, may be useful in diagnosis of early sepsis and determining prognosis

Imaging modalities that may be helpful include the following:

  • Chest radiography (to rule out pneumonia and diagnose other causes of pulmonary infiltrates)
  • Abdominal ultrasonography (for suspected biliary tract obstruction)
  • Abdominal CT or MRI (for assessing a suspected nonbiliary intra-abdominal source of infection or delineating intrarenal and extrarenal pathology)

The following cardiac studies may be useful if acute myocardial infarction (MI) is likely:

  • Electrocardiography (ECG)
  • Cardiac enzyme levels

Invasive diagnostic procedures that may be considered include the following:

  • Thoracentesis (in patients with substantial pleural effusion)
  • Paracentesis (in patients with gross ascites)
  • Swan-Ganz catheterization (for helping manage fluid status and assessing left ventricular dysfunction in MI; not for diagnosis of sepsis per se)

See Workup for more detail.

Management

Initial management may include the following:

  • Bed rest or admission to the ICU for monitoring and treatment
  • Transfer if requisite facilities are not available at the admitting hospital
  • Initiation of empiric antibiotic therapy, to be followed by focused treatment
  • Supportive therapy as necessary to maintain organ perfusion and respiration

Appropriate antimicrobial therapy depends on adequate coverage of the resident flora of the organ system presumed to be the source of the septic process and potential antimicrobial resistance patterns as follows:

  • IV line infections – Meropenem or cefepime plus additional coverage for staphylococci; if MRSA is prevalent, addition of linezolid, vancomycin, or daptomycin; if methicillin-sensitive staphylococci are recovered, avoidance of vancomycin if possible; line removal
  • Biliary tract infections – Imipenem, meropenem, piperacillin-tazobactam, or ampicillin-sulbactam
  • Intra-abdominal and pelvic infections – Imipenem, meropenem, piperacillin-tazobactam, ampicillin-sulbactam, or tigecycline; clindamycin or metronidazole plus aztreonam, levofloxacin, or an aminoglycoside
  • Urosepsis – Aztreonam, levofloxacin, a third- or fourth-generation cephalosporin, or an aminoglycoside; for enterococci, ampicillin or vancomycin; for vancomycin-resistant enterococcal urosepsis, linezolid or daptomycin; for community-acquired urosepsis, levofloxacin, aztreonam, or an aminoglycoside plus ampicillin; for nosocomial urosepsis, piperacillin, imipenem, or meropenem
  • Pneumococcal sepsis – Certain third-generation cephalosporins, carbapenem, or vancomycin if resistance is suspected
  • Sepsis of unknown origin – Meropenem, imipenem, piperacillin-tazobactam, or tigecycline; metronidazole plus either levofloxacin, aztreonam, cefepime, or ceftriaxone

Early surgical evaluation for presumed intra-abdominal or pelvic sepsis is essential. Procedures that may be warranted depend on the source of the infection, the severity of sepsis, and the patient’s clinical status, among other factors.

See Treatment and Medication for more detail.

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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 a subset of sepsis in which underlying circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than sepsis alone (identified using the clinical criteria of hypotension requiring vasopressor therapy to maintain mean blood pressure of 65 mm Hg or greater and having a serum lactate level >2 mmol/L after adequate fluid resuscitation).[2, 3]

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 Sepsis (Blood Infection).

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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.[1] 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.[2] An abdominal wall abscess is depicted on the CT scan depicted below.

A right lower quadrant abdominal wall abscess and 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.

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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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Contributor Information and Disclosures
Author

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of Ohio, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Department of Internal Medicine, Director of Infectious Disease Fellowship, Harper Hospital, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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A right lower quadrant abdominal wall abscess and enteric fistula are observed and confirmed by the presence of enteral contrast in the abdominal wall.
Table 1. Clinical Conditions Associated With Sepsis
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]
Table 2. Noninfectious Conditions Mimicking Clinical and Hemodynamic Parameters of Sepsis
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  
Table 3. Characteristics of Pseudosepsis and Sepsis
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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