Sepsis overview: Difference between revisions
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==Overview== | ==Overview== | ||
Sepsis is a serious medical condition characterized by a whole-body [[Inflammation|inflammatory]] state caused by [[infection]]. | Sepsis is a serious medical condition characterized by a whole-body [[Inflammation|inflammatory]] state caused by [[infection]]. | ||
Traditionally the term sepsis has been used interchangeably with septicaemia and septicemia ("blood poisoning"). However, these terms are no longer considered synonymous; septicemia is considered a subset of sepsis. [[Septic shock]] is a serious [[medicine|medical]] condition caused by decreased tissue perfusion and oxygen delivery as a result of [[infection]] and [[sepsis]]. It can cause [[multiple organ failure]] and [[death]]. Its most common victims are children, [[immunodeficiency|immunocompromised]] individuals, and the elderly. This is because their [[immune system]]s cannot cope with the infection as well as those of full-grown adults. | Traditionally the term sepsis has been used interchangeably with septicaemia and septicemia ("blood poisoning"). However, these terms are no longer considered synonymous; septicemia is considered a subset of sepsis. [[Septic shock]] is a serious [[medicine|medical]] condition caused by decreased tissue perfusion and oxygen delivery as a result of [[infection]] and [[sepsis]]. It can cause [[multiple organ failure]] and [[death]]. Its most common victims are children, [[immunodeficiency|immunocompromised]] individuals, and the elderly. This is because their [[immune system]]s cannot cope with the infection as well as those of full-grown adults.<ref name="pmid23983879">{{cite journal |vauthors=Karnatovskaia LV, Festic E |title=Sepsis: a review for the neurohospitalist |journal=Neurohospitalist |volume=2 |issue=4 |pages=144–53 |year=2012 |pmid=23983879 |pmc=3726110 |doi=10.1177/1941874412453338 |url=}}</ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
The immunological response that causes sepsis is a systemic inflammatory response causing widespread activation of [[inflammation]] and [[coagulation]] pathways. This may progress to dysfunction of the [[septic shock|circulatory system]] and, even under optimal treatment, may result in the [[multiple organ dysfunction syndrome]] and eventually [[death]]. A subclass of [[distributive shock]], shock refers specifically to decreased tissue [[perfusion]] resulting in end-organ dysfunction. [[Cytokines]] [[TNFα]], [[interleukin|IL]]-1β, [[interferon]] γ, [[interleukin|IL]]-6 released in a large scale inflammatory response results in massive [[vasodilation]], increased [[capillary]] permeability, decreased systemic vascular resistance, and [[hypotension]]. Hypotension reduces tissue perfusion pressure and thus tissue [[Hypoxia (medical)|hypoxia]] ensues. Finally, in an attempt to offset decreased [[blood pressure]], [[ventricular]] dilatation and [[myocardium|myocardial]] dysfunction will occur.<ref name="pmid28448952">{{cite journal |vauthors=Minasyan H |title=Sepsis and septic shock: Pathogenesis and treatment perspectives |journal=J Crit Care |volume=40 |issue= |pages=229–242 |year=2017 |pmid=28448952 |doi=10.1016/j.jcrc.2017.04.015 |url=}}</ref><ref name="pmid25870671">{{cite journal |vauthors=Pop-Began V, Păunescu V, Grigorean V, Pop-Began D, Popescu C |title=Molecular mechanisms in the pathogenesis of sepsis |journal=J Med Life |volume=7 Spec No. 2 |issue= |pages=38–41 |year=2014 |pmid=25870671 |pmc=4391358 |doi= |url=}}</ref><ref name="pmid20887193">{{cite journal |vauthors=Stearns-Kurosawa DJ, Osuchowski MF, Valentine C, Kurosawa S, Remick DG |title=The pathogenesis of sepsis |journal=Annu Rev Pathol |volume=6 |issue= |pages=19–48 |year=2011 |pmid=20887193 |pmc=3684427 |doi=10.1146/annurev-pathol-011110-130327 |url=}}</ref><ref name="pmid14767363">{{cite journal |vauthors=Cunneen J, Cartwright M |title=The puzzle of sepsis: fitting the pieces of the inflammatory response with treatment |journal=AACN Clin Issues |volume=15 |issue=1 |pages=18–44 |year=2004 |pmid=14767363 |doi= |url=}}</ref><ref name="pmid24292568">{{cite journal |vauthors=Chaudhry H, Zhou J, Zhong Y, Ali MM, McGuire F, Nagarkatti PS, Nagarkatti M |title=Role of cytokines as a double-edged sword in sepsis |journal=In Vivo |volume=27 |issue=6 |pages=669–84 |year=2013 |pmid=24292568 |pmc=4378830 |doi= |url=}}</ref> | The immunological response that causes sepsis is a systemic inflammatory response causing widespread activation of [[inflammation]] and [[coagulation]] pathways. This may progress to dysfunction of the [[septic shock|circulatory system]] and, even under optimal treatment, may result in the [[multiple organ dysfunction syndrome]] and eventually [[death]]. A subclass of [[distributive shock]], shock refers specifically to decreased tissue [[perfusion]] resulting in end-organ dysfunction. [[Cytokines]] [[TNFα]], [[interleukin|IL]]-1β, [[interferon]] γ, [[interleukin|IL]]-6 released in a large scale inflammatory response results in massive [[vasodilation]], increased [[capillary]] permeability, decreased systemic vascular resistance, and [[hypotension]]. Hypotension reduces tissue perfusion pressure and thus tissue [[Hypoxia (medical)|hypoxia]] ensues. Finally, in an attempt to offset decreased [[blood pressure]], [[ventricular]] dilatation and [[myocardium|myocardial]] dysfunction will occur.<ref name="pmid28448952">{{cite journal |vauthors=Minasyan H |title=Sepsis and septic shock: Pathogenesis and treatment perspectives |journal=J Crit Care |volume=40 |issue= |pages=229–242 |year=2017 |pmid=28448952 |doi=10.1016/j.jcrc.2017.04.015 |url=}}</ref><ref name="pmid25870671">{{cite journal |vauthors=Pop-Began V, Păunescu V, Grigorean V, Pop-Began D, Popescu C |title=Molecular mechanisms in the pathogenesis of sepsis |journal=J Med Life |volume=7 Spec No. 2 |issue= |pages=38–41 |year=2014 |pmid=25870671 |pmc=4391358 |doi= |url=}}</ref><ref name="pmid20887193">{{cite journal |vauthors=Stearns-Kurosawa DJ, Osuchowski MF, Valentine C, Kurosawa S, Remick DG |title=The pathogenesis of sepsis |journal=Annu Rev Pathol |volume=6 |issue= |pages=19–48 |year=2011 |pmid=20887193 |pmc=3684427 |doi=10.1146/annurev-pathol-011110-130327 |url=}}</ref><ref name="pmid14767363">{{cite journal |vauthors=Cunneen J, Cartwright M |title=The puzzle of sepsis: fitting the pieces of the inflammatory response with treatment |journal=AACN Clin Issues |volume=15 |issue=1 |pages=18–44 |year=2004 |pmid=14767363 |doi= |url=}}</ref><ref name="pmid24292568">{{cite journal |vauthors=Chaudhry H, Zhou J, Zhong Y, Ali MM, McGuire F, Nagarkatti PS, Nagarkatti M |title=Role of cytokines as a double-edged sword in sepsis |journal=In Vivo |volume=27 |issue=6 |pages=669–84 |year=2013 |pmid=24292568 |pmc=4378830 |doi= |url=}}</ref> | ||
Revision as of 16:08, 23 May 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]
Synonyms and keywords: sepsis syndrome; septic shock; septicemia
Overview
Sepsis is a serious medical condition characterized by a whole-body inflammatory state caused by infection. Traditionally the term sepsis has been used interchangeably with septicaemia and septicemia ("blood poisoning"). However, these terms are no longer considered synonymous; septicemia is considered a subset of sepsis. Septic shock is a serious medical condition caused by decreased tissue perfusion and oxygen delivery as a result of infection and sepsis. It can cause multiple organ failure and death. Its most common victims are children, immunocompromised individuals, and the elderly. This is because their immune systems cannot cope with the infection as well as those of full-grown adults.[1]
Pathophysiology
The immunological response that causes sepsis is a systemic inflammatory response causing widespread activation of inflammation and coagulation pathways. This may progress to dysfunction of the circulatory system and, even under optimal treatment, may result in the multiple organ dysfunction syndrome and eventually death. A subclass of distributive shock, shock refers specifically to decreased tissue perfusion resulting in end-organ dysfunction. Cytokines TNFα, IL-1β, interferon γ, IL-6 released in a large scale inflammatory response results in massive vasodilation, increased capillary permeability, decreased systemic vascular resistance, and hypotension. Hypotension reduces tissue perfusion pressure and thus tissue hypoxia ensues. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction will occur.[2][3][4][5][6]
Causes
The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. In rough order of severity, these are bacteremia or fungemia; septicemia; sepsis, severe sepsis or sepsis syndrome; septic shock; refractory septic shock; multiple organ dysfunction syndrome, and death. The condition develops as a response to certain microbial molecules which trigger the production and release of cellular mediators, such as tumor necrosis factors (TNF); these act to stimulate immune response.
Differentiating Sepsis from other Diseases
Sepsis must be differentiated from other syndromes such as the acute bacterial endocarditis, myocardial ring abscess, subacute bacterial endocarditis, pharyngitis, sinusitis, bronchitis, otitis media, and bacterial meningitis.
Epidemiology and Demographics
The hospitalization rate of those with a principal diagnosis of septicemia or sepsis more than doubled from 2000 through 2008. During the same period, the hospitalization rate for those with septicemia or sepsis as a principal or as a secondary diagnosis increased by 70% from 221 to 377 for every 100,000 people. Reasons for these increases may include an aging population with more chronic illnesses, greater use of invasive procedures, immunosuppressive drugs, chemotherapy, transplantation, and increasing microbial resistance to antibiotics.[7]
Risk Factors
Factors responsible for increased risk of sepsis may include an aging population with more chronic illnesses; greater use of invasive procedures, immunosuppressive drugs, chemotherapy, and transplantation; and increasing microbial resistance to antibiotics.[7] Other patients population at increased risk are ICU admits, immunocompromised, bacteremic, with community acquired pneumonia, and with genetic predisposition.
Natural History, Complications and Prognosis
There are many complications associated with sepsis, especially because it is a systemic phenomenon. Sepsis is a severe condition, and the prognosis of the patient will depend greatly on the condition and overall health of the patient. Many factors, such as age, hosts immune response, site of infection, type of infection, appropriate antibiotic therapy, and restoration of circulation of perfusion contribute to the overall prognosis.
Diagnosis
Physical Examination
The physical examination of sepsis shows findings of the causative system as well as some generalized features.
Laboratory Findings
The international guideline committee for diagnosis of septic shock recommends obtaining appropriate cultures that may include at least two blood cultures, urine, cerebrospinal fluid, wounds, respiratory secretions, or other body fluid cultures before antimicrobial therapy is initiated. If such cultures do not cause significant delay in antibiotic administration, then other tests that may be done include blood gases, kidney function tests, platelet count, white blood cell count, blood differential, fibrin degradation products, and peripheral smear.
Chest X Ray
The chest x ray may show the features consistent with the primary source of infection.
CT
The CT may show the features consistent with the primary source of infection.
MRI
The MRI may show the features consistent with the primary source of infection.
Echocardiography or Ultrasound
The echocardiography or ultrasound may show the features consistent with the primary source of infection.
Treatment
Medical Therapy
The "Surviving Sepsis Campaign" was an international effort organized by physicians that developed and promoted widespread adoption of practice improvement programs grounded in evidence-based guidelines. The goal was to improve diagnosis and treatment of sepsis. Included among the guidelines were sepsis screening for high-risk patients; taking bacterial cultures soon after the patient arrived at the hospital; starting patients on broad-spectrum intravenous antibiotic therapy before the results of the cultures are obtained; identifying the source of infection and taking steps to control it (e.g., abscess drainage); administering intravenous fluids to correct a loss or decrease in blood volume; and maintaining glycemic (blood sugar) control. These and similar guidelines have been tested by a number of hospitals and have shown potential for decreasing hospital mortality due to sepsis.[7][8]
Surgery
Surgical intervention is not recommended for the management of sepsis
Prevention
Prevent infections that can lead to sepsis by cleaning scrapes and wounds and getting regular vaccination against infections that cause sepsis can help in the prevention of sepis.
References
- ↑ Karnatovskaia LV, Festic E (2012). "Sepsis: a review for the neurohospitalist". Neurohospitalist. 2 (4): 144–53. doi:10.1177/1941874412453338. PMC 3726110. PMID 23983879.
- ↑ Minasyan H (2017). "Sepsis and septic shock: Pathogenesis and treatment perspectives". J Crit Care. 40: 229–242. doi:10.1016/j.jcrc.2017.04.015. PMID 28448952.
- ↑ Pop-Began V, Păunescu V, Grigorean V, Pop-Began D, Popescu C (2014). "Molecular mechanisms in the pathogenesis of sepsis". J Med Life. 7 Spec No. 2: 38–41. PMC 4391358. PMID 25870671.
- ↑ Stearns-Kurosawa DJ, Osuchowski MF, Valentine C, Kurosawa S, Remick DG (2011). "The pathogenesis of sepsis". Annu Rev Pathol. 6: 19–48. doi:10.1146/annurev-pathol-011110-130327. PMC 3684427. PMID 20887193.
- ↑ Cunneen J, Cartwright M (2004). "The puzzle of sepsis: fitting the pieces of the inflammatory response with treatment". AACN Clin Issues. 15 (1): 18–44. PMID 14767363.
- ↑ Chaudhry H, Zhou J, Zhong Y, Ali MM, McGuire F, Nagarkatti PS, Nagarkatti M (2013). "Role of cytokines as a double-edged sword in sepsis". In Vivo. 27 (6): 669–84. PMC 4378830. PMID 24292568.
- ↑ 7.0 7.1 7.2 "Products - Data Briefs - Number 62 - June 2011". Retrieved 2012-09-17.
- ↑ Wiedermann CJ, Adamson IY, Pert CB, Bowden DH. "Enhanced secretion of immunoreactive bombesin by alveolar macrophages exposed to silica". Journal of Leukocyte Biology. 43 (2): 99–103. PMID 2826633. Retrieved 2012-09-17.