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Sepsis

Sepsis (in Greek Σήψις, putrefaction) is a serious medical condition caused by a severe infection. The more critical subsets of sepsis include severe sepsis (sepsis with acute organ dysfunction) and septic shock (sepsis with refractory arterial hypotension). If a proven source of infection is lacking but the other criteria of sepsis are met the condition is known as systemic inflammatory response syndrome. more...

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Septicemia is sepsis of the bloodstream caused by bacteremia, which is the presence of bacteria in the bloodstream. The term septicemia is also used to refer to sepsis in general.

Symptoms

The systemic inflammatory response leads to widespread activation of inflammation and coagulation pathways. This may progress to dysfunction of the circulatory system and, even under optimal treatment, multiple organ dysfunction syndrome and eventually death.

Sepsis is common and also more dangerous in elderly, immunocompromised, and critically ill patients. It occurs in 2% of all hospitalizations and accounts for as much as 25% of intensive care unit (ICU) bed utilization. It is a major cause of death in intensive care units worldwide, with mortality rates that range from 20% for sepsis to 40% for severe sepsis to >60% for septic shock. In the United States, sepsis is the leading cause of death in non-coronary ICU patients, and the tenth most common cause of death overall according to 2000 data from the Centers for Disease Control and Prevention.

A problem in the adequate management of septic patients has been the delay in administering the right treatment after sepsis has been recognized. A large international collaboration was established to educate people about sepsis and to improve patient outcomes with sepsis, entitled the "Surviving Sepsis Campaign." The Campaign has published an evidence-based review of management strategies for severe sepsis, with the aim to publish a complete set of guidelines within 3 years.

Definition of sepsis

Sepsis can be diagnosed if there is a proven source of infection, such as a positive blood culture and two or more of the following:

  • Heart rate > 90 beats per minute
  • Body temperature < 36 (96.8°F) or > 38°C (100.4°F)
  • Hyperventilation (high respiratory rate) > 20 breaths per minute or, on blood gas, a PaCO2 less than 32 mm Hg
  • White blood cell count < 4000 cells/mm³ or > 12000 cells/mm³ (< 4 x 109 or > 12 x 109 cells/L).

Treatment

The therapy of sepsis rests on antibiotics, surgical drainage of infected fluid collections, fluid replacement and appropriate support for organ dysfunction. This may include hemodialysis in kidney failure, mechanical ventilation in pulmonary dysfunction, transfusion of blood plasma, platelets and coagulation factors to stabilize blood coagulation, and drug and fluid therapy for circulatory failure. Ensuring adequate nutrition, if necessary by parenteral nutrition, is important during prolonged illness.

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Uninfected systemic inflammatory response syndrome or future sepsis? differences in extracellular matrix modulators prior to onset of clinical sepsis
From CHEST, 10/1/05 by Steven B. Johnson

PURPOSE: Inflammation and sepsis induce changes in the extracellular matrix (ECM). ECM degradation and deposition is tightly controlled by matrix metalloproteinases (MMP) and their inhibitors, tissue inhibitors of metalloproteinase (TIMP) respectively. TIMP are multifunctional, participating in anti-apoptotic activity, B cell differentiation, and IL-10 production. We hypothesize that differential expression of TIMP-I and MMP-9 occurs in SIRS patients that remain uninfected compared to those who subsequently become infected and that these differences occur prior to onset of clinical sepsis.

METHODS: Longitudinal blood samples were collected on critically ill non-infected SIRS patients and analyzed for MMP-9 and TIMP-1. SIRS patients who subsequently converted to sepsis (Pre-septic SIRS) were time matched to patients who remained uninfected (Non-septic SIRS). Comparisons between the 2 groups occurred at study entry, and at 60 hours prior (T-60), 36 hours prior (T-36), and 12 hours prior (T-12) to onset of microbiologically proven clinical sepsis. MMP-9 and TIMP-1 were measured by immunoassay. Data expressed as mean [+ or -] SD.

RESULTS: 50 Pre-septic SIRS patients and 47 Non-septic SIRS patients were compared at each time point (see table). TIMP-1 levels were significantly higher in the pre-septic SIRS patients. MMP-9 levels were similar in both groups until Pre-septic elevated at T-12. MMP-9/ TIMP-1 ratios were lower in the Pre-septic patients initially but sequentially increased becoming significantly elevated at T-12 prior to clinical sepsis.

CONCLUSION: ECM undergoes dynamic modulation with changes in MMP-9/TIMP-1 ratio prior to conversion from SIRS to sepsis. Elevated TIMP-1 levels occur early, more than 60 hours before clinical sepsis. In addition, TIMP-1 appears dissociated from MMP-9 suggesting alternative activation and functions in SIRS patients who subsequently convert to sepsis.

CLINICAL IMPLICATIONS: Earlier diagnosis of sepsis in SIRS patients may be possible by evaluating modulators of the extracellular matrix.

DISCLOSURE: Steven Johnson, Grant monies (from industry related sources) Research Grant Support from BD Diagnostics, Baltimore Maryland; Glaxo SmithKline; Wyeth; Consultant fee, speaker bureau, advisory committee, etc. GlaxoSmithKline; Wyeth; Lilly.

Steven B. Johnson MD * Grant Bochicchio MD Carl Shanholtz MD Alan Cross MD Jeff Hasday MD Michael Townes MD Richard Moore MD Thomas Scalea MD R. Adams Cowley Shock Trauma Center, Baltimore, MD

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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