What is sepsis and what is its clinical progression?

Answer

Sepsis is a clinical syndrome that complicates severe infection and is characterized by systemic inflammation and widespread tissue injury. A continuum of severity from sepsis to septic shock and MODS exists. The clinical process usually begins with infection, which potentially leads to sepsis and organ dysfunction.^[2]A consensus panel of the American College of Chest Physicians and the Society of Critical Care Medicine developed definitions of the various stages of this process (see the image below).^[3]

Stages of sepsis based on American College of Chest Physicians/Society of Critical Care Medicine Consensus Panel guidelines.

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Infection is usually a microbial phenomenon in which an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by these organisms is characteristic. However, viral infections can be indistinguishable from bacteria infections in their presentation.

Bacteremia is the presence of viable bacteria in the blood.

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Media Gallery

Stages of sepsis based on American College of Chest Physicians/Society of Critical Care Medicine Consensus Panel guidelines.
Pathogenesis of sepsis and multiorgan failure.
Venn diagram showing overlap of infection, bacteremia, sepsis, systemic inflammatory response syndrome (SIRS), and multiorgan dysfunction.
Acute respiratory distress syndrome (ARDS) present in this chest x-ray (CXR) film is a common organ system affected in multiorgan failure of sepsis.
Acute respiratory distress syndrome (ARDS) shown in this chest x-ray (CXR) film is a common complication of septic shock. Note bilateral airspace infiltration, absence of cardiomegaly, vascular redistribution, and Kerley B lines.
Organizing phase of diffuse alveolar damage (ARDS) secondary to septic shock shows diffuse alveolar injury and infiltration with inflammatory cells.
Organizing diffuse alveolar damage in a different location showing disorganization of pulmonary architecture.
A high-power view of organizing diffuse alveolar damage (ARDS) shows hyperplasia of type II pneumocytes and hyaline membrane deposits.

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Author

Ali H Al-Khafaji, MD, MPH, FACP, FCCP, FCCM Professor of Critical Care Medicine, Professor of Surgery, University of Pittsburgh School of Medicine; Medical Director, Transplant Intensive Care Unit, Medical Director, ICU Telemedicine, Department of Critical Care Medicine, University of Pittsburgh Medical Center

Ali H Al-Khafaji, MD, MPH, FACP, FCCP, FCCM is a member of the following medical societies: Allegheny County Medical Society, American College of Chest Physicians, American College of Gastroenterology, American Medical Association, American Thoracic Society, British Medical Association, International Liver Transplantation Society, Royal College of Anaesthetists, Society of Critical Care Anesthesiologists, Society of Critical Care Medicine, Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba Faculty of Medicine; Site Director, Respiratory Medicine, St Boniface General Hospital, Canada

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

Gregg Eschun, MD Assistant Professor, Department of Internal Medicine, Sections of Respirology and Critical Care, St Boniface Hospital, University of Manitoba Faculty of Medicine, Canada

Gregg Eschun, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Canadian Medical Association, College of Physicians and Surgeons of Manitoba

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease, Clinical and Translational Science and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Thoracic Society, European Society of Intensive Care Medicine, Society of Critical Care Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Baxter Medical, Exostat, LiDCO<br/>Received honoraria from LiDCO Ltd for consulting; Received intellectual property rights from iNTELOMED.

Acknowledgements

Cory Franklin, MD Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science; Director, Division of Critical Care Medicine, Cook County Hospital

Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic 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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