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Sepsis or Septicemia
Classification and external resources
ICD-10 A40. - A41.0
ICD-9 995.91
DiseasesDB 11960
MedlinePlus 000666
MeSH D018805

Sepsis is a serious medical condition that is characterized by a whole-body inflammatory state (called a systemic inflammatory response syndrome or SIRS) and the presence of a known or suspected infection.[1][2] The body may develop this inflammatory response to microbes in the blood, urine, lungs, skin, or other tissues. A lay term for sepsis is blood poisoning, more aptly applied to septicemia, below.

Septicemia (also septicaemia or septicæmia [sep⋅ti⋅cæ⋅mi⋅a][3], or erroneously septasemia and septisema) is a related but deprecated (formerly sanctioned) medical term referring to the presence of pathogenic organisms in the bloodstream, leading to sepsis.[4] The term has not been sharply defined. It has been inconsistently used in the past by medical professionals, for example as a synonym of bacteremia, causing some confusion. The present medical consensus is therefore that the term "septicemia" is problematic and should be avoided.[2]

Sepsis is usually treated in the intensive care unit with intravenous fluids and antibiotics. If fluid replacement is insufficient to maintain blood pressure, specific vasopressor medications can be used. Artificial ventilation and dialysis may be needed to support the function of the lungs and kidneys, respectively. To guide therapy, a central venous catheter and an arterial catheter may be placed. Sepsis patients require preventive measures for deep vein thrombosis, stress ulcers and pressure ulcers, unless other conditions prevent this. Some patients might benefit from tight control of blood sugar levels with insulin (targeting stress hyperglycemia), low-dose corticosteroids or activated drotrecogin alfa (recombinant protein C).[5]

Contents

Terminology

Severe sepsis occurs when sepsis leads to organ dysfunction, low blood pressure (hypotension), or insufficient blood flow (hypoperfusion) to one or more organs (causing, for example, lactic acidosis, decreased urine production, or altered mental status). Sepsis can lead to septic shock, multiple organ dysfunction syndrome (formerly known as multiple organ failure), and death. Organ dysfunction results from sepsis-induced hypotension (< 90 mmHg or a reduction of ≥ 40 mmHg from baseline) and diffuse intravascular coagulation, among other things.

Bacteremia is the presence of viable bacteria in the bloodstream. Likewise, the terms viremia and fungemia simply refer to viruses and fungi in the bloodstream. These terms say nothing about the consequences this has on the body. For example, bacteria can be introduced into the bloodstream during toothbrushing.[6] This form of bacteremia almost never causes problems in normal individuals. However, bacteremia associated with certain dental procedures can cause bacterial infection of the heart valves (known as endocarditis) in high-risk patients.[7] Conversely, a systemic inflammatory response syndrome can occur in patients without the presence of infection, for example in those with burns, polytrauma, or the initial state in pancreatitis and chemical pneumonitis.[2]

Signs and symptoms

In addition to symptoms related to the provoking infection, sepsis is characterized by evidence of acute inflammation present throughout the entire body, and is, therefore, frequently associated with fever and elevated white blood cell count (leukocytosis) or low white blood cell count and lower-than-average temperature, and vomiting[citation needed]. The modern concept of sepsis is that the host's immune response to the infection causes most of the symptoms of sepsis, resulting in hemodynamic consequences and damage to organs. This host response has been termed systemic inflammatory response syndrome (SIRS) and is characterized by hemodynamic compromise and resultant metabolic derangement. Outward physical symptoms of this response frequently include a high heart rate (above 100 beats per minute), high respiratory rate (above 20 breaths per minute), elevated WBC count (above 12,000) and elevated or lowered body temperature (under 36 °C or over 38 °C). Sepsis is differentiated from SIRS by the presence of a known pathogen. For example SIRS and a positive blood culture for a pathogen indicates the presence of sepsis. Without a known infection, it's not possible to classify the above symptoms as sepsis, only SIRS.

This immunological response causes widespread activation of acute-phase proteins, affecting the complement system and the coagulation pathways, which then cause damage to the vasculature as well as to the organs. Various neuroendocrine counter-regulatory systems are then activated as well, often compounding the problem. Even with immediate and aggressive treatment, this may progress to multiple organ dysfunction syndrome and eventually death.

Diagnosis

According to the American College of Chest Physicians and the Society of Critical Care Medicine[2], there are different levels of sepsis:

Examples of end-organ dysfunction include the following:[8]

More specific definitions of end-organ dysfunction exist for SIRS in pediatrics.[9]

  • Cardiovascular dysfunction (after fluid resuscitation with at least 40 ml/kg of crystalloid)
    • hypotension with blood pressure < 5th percentile for age or systolic blood pressure < 2 standard deviations below normal for age, OR
    • vasopressor requirement, OR
    • two of the following criteria:
  • Respiratory dysfunction (in the absence of cyanotic heart disease or known chronic lung disease)
    • the ratio of the arterial partial-pressure of oxygen to the fraction of oxygen in the gases inspired (PaO2/FiO2) < 300 (the definition of acute lung injury), OR
    • arterial partial-pressure of carbon dioxide (PaCO2) > 65 torr (20 mmHg) over baseline PaCO2 (evidence of hypercapnic respiratory failure), OR
    • supplemental oxygen requirement of greater than FiO2 0.5 to maintain oxygen saturation ≥ 92%
  • Neurologic dysfunction
  • Hematologic dysfunction
  • Renal dysfunction
  • Hepatic dysfunction (only applicable to infants > 1 month)

Consensus definitions, however, continue to evolve, with the latest expanding the list of signs and symptoms of sepsis to reflect clinical bedside experience.[10]

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Neonatal sepsis

In common clinical usage, sepsis specifically refers to the presence of a serious bacterial infection (SBI) (such as meningitis, pneumonia, pyelonephritis, or gastroenteritis) in the setting of fever. Criteria with regards to hemodynamic compromise or respiratory failure are not useful clinically because these symptoms often do not arise in neonates until death is imminent and unpreventable.

Treatment

Adults and children

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 products, and drug and fluid therapy for circulatory failure. Ensuring adequate nutrition—preferably by enteral feeding, but if necessary by parenteral nutrition—is important during prolonged illness.

A problem in the adequate management of septic patients has been the delay in administering therapy after sepsis has been recognized. Published studies have demonstrated that for every hour delay in the administration of appropriate antibiotic therapy there is an associated 7% rise in mortality. 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,[5] with the aim to publish a complete set of guidelines in subsequent years.

Early Goal Directed Therapy (EGDT), developed at Henry Ford Hospital by E. Rivers, MD, is a systematic approach to resuscitation that has been validated in the treatment of severe sepsis and septic shock. It is meant to be started in the Emergency Department. The theory is that one should use a step-wise approach, having the patient meet physiologic goals, to optimize cardiac preload, afterload, and contractility, thus optimizing oxygen delivery to the tissues.[11] A recent meta-analysis showed that EGDT provides a benefit on mortality in patients with sepsis.[12] As of December 2008 some controversy around its uses remains and a number of trials are ongoing in an attempt to resolve this.[13]

In EGDT, fluids are administered until the central venous pressure (CVP), as measured by a central venous catheter, reaches 8-12 cm of water (or 10-15 cm of water in mechanically ventilated patients). Rapid administration of several liters of isotonic crystalloid solution is usually required to achieve this. If the mean arterial pressure is less than 65 mmHg or greater than 90 mmHg, vasopressors or vasodilators are given as needed to reach the goal. Once these goals are met, the mixed venous oxygen saturation (SvO2), i.e., the oxygen saturation of venous blood as it returns to the heart as measured at the vena cava, is optimized. If the SvO2 is less than 70%, blood is given to reach a hemoglobin of 10 g/dl and then inotropes are added until the SvO2 is optimized. Elective intubation may be performed to reduce oxygen demand if the SvO2 remains low despite optimization of hemodynamics. Urine output is also monitored, with a minimum goal of 0.5 ml/kg/h. In the original trial, mortality was cut from 46.5% in the control group to 30.5% in the intervention group.[11] The Surviving Sepsis Campaign guidelines recommend EGDT for the initial resuscitation of the septic patient with a level B strength of evidence (single randomized control trial).[5]

Most therapies aimed at the inflammation process itself have failed to improve outcome, however drotrecogin alfa (activated protein C, one of the coagulation factors) has been shown to decrease mortality from about 31% to about 25% in severe sepsis. To qualify for drotrecogin alfa, a patient must have severe sepsis or septic shock with an APACHE II score of 25 or greater and a low risk of bleeding.[14]

During critical illness, a state of adrenal insufficiency and tissue resistance (the word 'relative' resistance should be avoided[15]) to corticosteroids may occur. This has been termed critical illness–related corticosteroid insufficiency.[15] Treatment with corticosteroids might be most beneficial in those with septic shock and early severe acute respiratory distress syndrome (ARDS), whereas its role in other patients such as those with pancreatitis or severe pneumonia is unclear.[15] These recommendations stem from studies showing benefits from low dose hydrocortisone treatment for septic shock patients and methylprednisolone in ARDS patients.[16][17][18][19][20][21] However, the exact way of determining corticosteroid insufficiency remains problematic. It should be suspected in those poorly responding to resuscitation with fluids and vasopressors. ACTH stimulation testing is not recommended to confirm the diagnosis.[15] Glucocorticoid drugs should be weaned and not stopped abruptly.

In some cases, sepsis may lead to inadequate tissue perfusion and necrosis. As this may affect the extremities, amputation may become necessary. On January 8 2009 a patent request was submitted for the possible treatment of sepsis ( 20090011974 Scavenger Receptor B1 (Cla-1) Targeting for the Treatment of Infection, Sepsis and Inflammation 01-08-2009) .

Neonates

Note that, in neonates, sepsis is difficult to diagnose clinically. They may be relatively asymptomatic until hemodynamic and respiratory collapse is imminent, so, if there is even a remote suspicion of sepsis, they are frequently treated with antibiotics empirically until cultures are sufficiently proven to be negative.

Prognosis

Prognosis can be estimated with the MEDS score.[22] Approximately 20–35% of patients with severe sepsis and 40–60% of patients with septic shock die within 30 days. Others die within the ensuing 6 months. Late deaths often result from poorly controlled infection, immunosuppression, complications of intensive care, failure of multiple organs, or the patient's underlying disease.

Prognostic stratification systems such as APACHE II indicate that factoring in the patient's age, underlying condition, and various physiologic variables can yield estimates of the risk of dying of severe sepsis. Of the individual covariates, the severity of underlying disease most strongly influences the risk of dying. Septic shock is also a strong predictor of short- and long-term mortality. Case-fatality rates are similar for culture-positive and culture-negative severe sepsis.

Some patients may experience severe long term cognitive decline following an episode of severe sepsis, but the absence of baseline neuropsychological data in most sepsis patients makes the incidence of this difficult to quantify or to study.[23] A preliminary study of nine patients with septic shock showed abnormalities in seven patients by MRI.[24]

Epidemiology

In the United States, sepsis is the second-leading cause of death in non-coronary ICU patients, and the tenth-most-common cause of death overall according to data from the Centers for Disease Control and Prevention (the first being heart disease).[25] Sepsis is common and also more dangerous in elderly, immunocompromised, and critically ill patients.[26] It occurs in 1–2% 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.

See also

References

  1. ^ Levy MM, Fink MP, Marshall JC, et al. (April 2003). "2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference". Crit. Care Med. 31 (4): 1250–6. doi:10.1097/01.CCM.0000050454.01978.3B. PMID 12682500. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0090-3493&volume=31&issue=4&spage=1250. 
  2. ^ a b c d Bone RC, Balk RA, Cerra FB, et al. (Jun 1992). "Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine". Chest 101 (6): 1644–55. doi:10.1378/chest.101.6.1644. PMID 1303622. http://www.chestjournal.org/content/101/6/1644. 
  3. ^ Dictionary
  4. ^ septicemia at eMedicine Dictionary
  5. ^ a b c Dellinger RP, Levy MM, Carlet JM, et al., for the International Surviving Sepsis Campaign Guidelines Committee. (2008). "Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008" (Subscription required). Crit Care Med 36 (1): 296–327. doi:10.1097/01.CCM.0000298158.12101.41. PMID 18158437. http://www.ccmjournal.com/pt/re/ccm/searchresults.htm. 
  6. ^ Lockhart PB, Brennan MT, Sasser HC, Fox PC, Paster BJ, Bahrani-Mougeot FK (Jun 2008). "Bacteremia associated with toothbrushing and dental extraction". Circulation 117 (24): 3118–25. doi:10.1161/CIRCULATIONAHA.107.758524. PMID 18541739. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=18541739. 
  7. ^ Wilson W, Taubert KA, Gewitz M, et al. (Oct 2007). "Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group". Circulation 116 (15): 1736–54. doi:10.1161/CIRCULATIONAHA.106.183095. PMID 17446442. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=17446442. 
  8. ^ Abraham E, Singer M (2007). "Mechanisms of sepsis-induced organ dysfunction" (Subscription required). Crit. Care Med. 35 (10): 2408–16. doi:10.1097/01.CCM.0000282072.56245.91. PMID 17948334. http://www.ccmjournal.com/pt/re/ccm/abstract.00003246-200710000-00026.htm. 
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  10. ^ Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, Cohen J, Opal SM, Vincent JL, Ramsay G (Apr 2003). "2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference". Crit Care Med 31 (4): 1250–1256. doi:10.1097/01.CCM.0000050454.01978.3B. http://www.ccmjournal.com/pt/re/ccm/abstract.00003246-200304000-00038.htm. 
  11. ^ a b Rivers E, Nguyen B, Havstad S, et al. (2001). "Early goal-directed therapy in the treatment of severe sepsis and septic shock". N. Engl. J. Med. 345 (19): 1368–77. doi:10.1056/NEJMoa010307. PMID 11794169. http://content.nejm.org/cgi/content/full/345/19/1368. 
  12. ^ Jones AE, Brown MD, Trzeciak S, et al. (October 2008). "The effect of a quantitative resuscitation strategy on mortality in patients with sepsis: a meta-analysis". Critical care medicine 36 (10): 2734–9. doi:10.1097/CCM.0b013e318186f839. PMID 18766093. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?doi=10.1097/CCM.0b013e318186f839. 
  13. ^ McKenna M (December 2008). "Controversy swirls around early goal-directed therapy in sepsis: pioneer defends ground- breaking approach to deadly disease". Ann Emerg Med 52 (6): 651–4. doi:10.1016/j.annemergmed.2008.10.013. PMID 19048659. 
  14. ^ Bernard GR, Vincent JL, Laterre PF, LaRosa SP, Dhainaut JF, Lopez-Rodriguez A, Steingrub JS, Garber GE, Helterbrand JD, Ely EW, Fisher CJ Jr (2001-03-08). "Recombinant human protein C Worldwide Evaluation in Severe Sepsis (PROWESS) study group. Efficacy and safety of recombinant human activated protein C for severe sepsis". N Engl J Med 344 (10): 699–709. doi:10.1056/NEJM200103083441001. PMID 11236773. http://content.nejm.org/cgi/content/abstract/344/10/699. 
  15. ^ a b c d Marik PE, Pastores SM, Annane D, et al. (Jun 2008). "Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: consensus statements from an international task force by the American College of Critical Care Medicine". Crit. Care Med. 36 (6): 1937–49. doi:10.1097/CCM.0b013e31817603ba. PMID 18496365. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?doi=10.1097/CCM.0b013e31817603ba. 
  16. ^ Annane D, Sebille V, Charpentier C, Bollaert PE, Francois B, Korach JM, Capellier G, Cohen Y, Azoulay E, Troche G, Chaumet-Riffaut P, Bellissant E (2002-08-21). "Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock". JAMA 288 (7): 862–71. doi:10.1001/jama.288.7.862. PMID 12186604. http://jama.ama-assn.org/cgi/content/full/288/7/862. 
  17. ^ Meduri GU, Headley AS, Golden E, et al. (Jul 1998). "Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial". JAMA 280 (2): 159–65. doi:10.1001/jama.280.2.159. PMID 9669790. http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=9669790. 
  18. ^ Meduri GU, Golden E, Freire AX, et al. (Apr 2007). "Methylprednisolone infusion in early severe ARDS: results of a randomized controlled trial". Chest 131 (4): 954–63. doi:10.1378/chest.06-2100. PMID 17426195. http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=17426195. 
  19. ^ Sprung CL, Annane D, Keh D, et al. (Jan 2008). "Hydrocortisone therapy for patients with septic shock". N. Engl. J. Med. 358 (2): 111–24. doi:10.1056/NEJMoa071366. PMID 18184957. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=18184957&promo=ONFLNS19. 
  20. ^ Steinberg KP, Hudson LD, Goodman RB, et al. (Apr 2006). "Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome". N. Engl. J. Med. 354 (16): 1671–84. doi:10.1056/NEJMoa051693. PMID 16625008. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=16625008&promo=ONFLNS19. 
  21. ^ Annane D, Sébille V, Bellissant E (Jan 2006). "Effect of low doses of corticosteroids in septic shock patients with or without early acute respiratory distress syndrome". Crit. Care Med. 34 (1): 22–30. doi:10.1097/01.CCM.0000194723.78632.62. PMID 16374152. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00003246-200601000-00004. 
  22. ^ Shapiro NI, Wolfe RE, Moore RB, Smith E, Burdick E, Bates DW (2003). "Mortality in Emergency Department Sepsis (MEDS) score: a prospectively derived and validated clinical prediction rule". Crit. Care Med. 31 (3): 670–5. doi:10.1097/01.CCM.0000054867.01688.D1. PMID 12626967. http://www.ccmjournal.com/pt/re/ccm/abstract.00003246-200303000-00002.htm. 
  23. ^ Jackson, J.; Hopkins, R.; Miller, R.; Gordon, S.; Wheeler, A.; Ely, E. (2009). "Acute respiratory distress syndrome, sepsis, and cognitive decline: a review and case study". Southern medical journal 102 (11): 1150–1157. doi:10.1097/SMJ.0b013e3181b6a592. PMID 19864995.  edit
  24. ^ Sharshar, T.; Carlier, R.; Bernard, F.; Guidoux, C.; Brouland, J.; Nardi, O.; De La Grandmaison, G.; Aboab, J. et al. (2007). "Brain lesions in septic shock: a magnetic resonance imaging study". Intensive care medicine 33 (5): 798–806. doi:10.1007/s00134-007-0598-y. PMID 17377766.  edit
  25. ^ Martin GS, Mannino DM, Eaton S, Moss M (2003-04-17). "The epidemiology of sepsis in the United States from 1979 through 2000". N Engl J Med 348 (16): 1546–54. doi:10.1056/NEJMoa022139. PMID 12700374. http://content.nejm.org/cgi/content/full/348/16/1546. 
  26. ^ "Sepsis can strike, kill shockingly fast" by Elizabeth Cohen, January 29, 2009, CNN

External links


1911 encyclopedia

Up to date as of January 14, 2010

From LoveToKnow 1911

Medical warning!
This article is from the 1911 Encyclopaedia Britannica. Medical science has made many leaps forward since it has been written. This is not a site for medical advice, when you need information on a medical condition, consult a professional instead.

SEPSIS (Gr. oiNits, putrefaction), Or Septic Infection, a term applied in medicine and surgery to indicate the resultant infection of a wound or sore by micro-organisms or by their products. Under this general heading come three great constitutional diseases, differing radically from each other in their aetiology and pathology: sapraemia, septicaemia and pyaemia. Sapraemia (Gr. aairpos, rotten, 21µa, blood), or septic intoxication, is the result of the absorption of a dose of the toxins produced by micro-organisms from some area of infection without the entrance of the micro-organisms themselves into the blood. This condition was for a long time confounded with septicaemia, but is distinguished from it in being a chemical intoxication. The blood in sapraemia if injected into an animal is incapable of reproducing the disease as in septicaemia. Any condition in which there is a mass of decomposing tissue in the neighbourhood of an unhealed wound may give rise to sapraemia. In surgical practice it may be met with in large, deep and badlydrained wounds where a quantity of putrifying material is pent up. When it arises in connexion with wounds accidentally received, it may be unavoidably due to the dirty state of the skin or to foreign bodies entering the wound. Absorption of toxins is notably frequent in portions of decomposing placental tissue which may accidentally have remained behind in the uterus after childbirth, and may give rise to puerperal sapraemia. Sapraemia is acute or subacute directly according to the amount of toxin absorbed. By some writers it is divided as follows: (i) Hectic fever is a chronic blood poisoning with continual absorption of small doses of the toxins. This variety usually arises in long-continued suppuration of bones and joints, and in decomposition occurring in a pulmonary cavity. The marked symptom is a sharp rise of temperature in the evenings; the face becomes flushed and the pulse rapid. After profuse sweating the temperature drops. Diarrhoea and wasting are a usual accompaniment. (2) Septic traumatic fever is a slight form which may follow burns or compound fractures and which tends to subside in a few days. (3) In acute septic intoxication large amounts of the poison are absorbed. It generally starts with a severe rigor followed by a continuous high temperature, dry tongue, rapid pulse and severe headache, together with nausea and vomiting, and in the later stages diarrhoea. If the case be a severe one rapid prostration speedily comes on with low muttering delirium, the temperature may fall to subnormal, and a gradually deepening coma may end in death; other cases pass into a typically "typhoid state," death occurring from exhaustion at the end of about a week. (4) Amyloid (Gr. ti j wXov, starch, e1.80s, form), or lardaceous disease, usually of the liver, spleen, kidneys or other organs, is one of the results of long-continued septic intoxication. A substance derived from the breaking down of pus and tissue cells is carried in the blood and deposited in the connective tissue of the coats of the smaller arteries, and the viscera become infiltrated with a material looking like lard. The liver and spleen, being the organs most usually affected, become immensely enlarged.

No form of septic infection yields so easily to treatment as sapraemia. The prompt removal of the cause of septic absorption, the flushing out of the wound with weak antiseptic solutions, in order to mechanically remove any decomposing masses, and the establishment of proper drainage in deep wounds, is usually followed by a fall in temperature and an improvement in the general condition. A strong, preferably mercurial, purgative should be given to aid in the elimination of toxic material. For the same purpose the injection into the veins or into the cellular tissue of large quantities of normal saline solution is useful. Heart depression should be overcome by diffusible stimulants and hypodermic injections of strychnine. When the wound has become "surgically clean" recovery is usually rapid.

Septicaemia is an acute infective disease differing from sapraemia in that the micro-organisms themselves are absorbed, entering the general circulation, and may on examination be found in greater or lesser number in the blood-stream itself. The organism or organisms grow and reproduce themselves in the blood or tissues. A number of different organisms have been isolated from the blood-stream in cases of septicaemia. The most frequently found is the Streptococcus pyogenes, which is present in 50% of the cases and is common in puerperal septicaemia and in ulcerative endocarditis. The Staphylococcus pyo genes aureus et albus is also a frequent cause, but sometimes septicaemia may be due to other pathogenic microbes such as the Pneumococcus, the Bacillus coli communis, Bacillus pyocyaneus, Bacillus oedematis maligni and the Gonococcus. The micro-organisms are conveyed by the blood-stream to different parts of the body, in which as in the original wound itself they both multiply and set up factories for the production of toxins. The disease commonly follows blows or wounds which have not been treated on surgical lines. Much laceration of the tissues at the time of the injury offers increased liability to infection. Septicaemia is frequent in spreading gangrene, in diseases of the periosteum, and in fevers such as scarlatina, diphtheria or plague, and in the puerperal state. The period of incubation may be from a few hours to several days. The condition of the wound or site of injury shows marked changes. In severe cases following a prick received in conducting a post-mortem the finger in a few hours becomes greatly swollen and painful, the pain spreading up the lymphatic vessels to the nearest lymphatic glands, which may become enlarged, and sloughing or gangrene of the parts involved may take place. In milder cases the wound remains with reddened and oedematous margins in a more or less unhealthy state. In mild cases of septicaemia the local condition of the wound, high temperature and feeling of illness are the distinguishing features. The treatment of septicaemia may be preventive or active. The preventive side consists in the performance of operations with all due aseptic precautions. Since the days when I. P. Semmel.weiss (q.v.) of Vienna insisted on cleanliness in his maternity wards, the death-rate of puerperal septicaemia has been enormously reduced. In the British registrar-general's returns for 1868 it was stated that in twenty-two years no less than 23,689 women in England and Wales had died of puerperal septic diseases. In the reports of the Rotunda Hospital, Dublin, the largest maternity hospital in the United Kingdom, we ascertain that of 30,023 women delivered during the ten years 1894-1903 there was only a mortality of 21 due to sepsis, a ratio of 0.066%, while the registrar-general's returns for England and Ireland for the period have a ratio for sepsis of 0.216%. When dealing with a wound that is already septic, free incision and swabbing the surface with pure carbolic acid may have to be resorted to, and constitutional treatment must be undertaken at once. Should the infection be due to a Streptococcus, an antistreptococcic serum may be injected. There are, however, many strains of Streptococci, and a polyvalent serum may give good results. Menzer's antistreptococcic serum has been successful in puerperal septicaemia not of gonococcic origin. Many cases have also now been recorded in which the systemic infection is combated by means of an autogenous vaccine. The first case was described by Sir James Barr before the Liverpool Medical Institute in May 1906. In urgent cases, where time will not allow of the manufacture of a vaccine, quinine in large doses, stimulants and liquid nourishment must be given, and the temperature controlled by tepid sponging.

Pyaemia (Gr. rbov, pus, aiya, blood), which got its name from an erroneous idea that the pus passed into the blood, is now understood to mean an acute disease with the formation of metastatic abscesses. The first definite account of the disease was published by Boerhaave in 1720. Virchow in 1846 pointed out that it was not pus in the veins, but altered blood-clot. Jean D'Arcet showed the separate processes of poisoning by products of decomposition and the blocking of the veins with emboli. Any pyogenic organism may give rise to pyaemia, or it may follow any acute abscess. The cause of pyaemia may be said to be any condition favouring the formation of emboli. An occasional cause of pyaemia is infective endocarditis, while puerperal pyaemia may arise from infection of the genital tract. When the emboli lodge in the lung there is a breaking down of the tissue in front of the embolus, a haemorrhagic infarct being formed. The clinical symptoms of acute pyaemia generally start with a rigor repeated at periodic intervals; the skin becomes hot and the patient soon develops an earthy colour, the pulse becomes frequent and weak and the tongue dry. In about a week secondary abscesses appear, most frequently in the region of joints. There may be little or no pain to herald the formation of an abscess, but usually there is intense pain followed by suppuration. Unless early treatment is undertaken the joint may be rapidly destroyed. In acute cases multiple abscesses in the kidney may give rise to pain and albuminuria, abscesses in the lungs to dyspnoea, while acute peritonitis may arise from rupture of a splenic abscess into the peritoneal cavity, and sudden blindness be the result of the plugging of the arteria centralis retinae. The duration of a case of pyaemia depends on the severity of the infection. Death may occur from the formation of abscesses in vital organs such as the brain and heart, or from exhaustion from continued suppuration, or chronic forms may after months pass on to complete recovery. Unfortunately pyaemia cannot be recognized apart from other blood infections until abscesses begin to form. The local treatment is to endeavour to prevent the detachment of infected emboli and the infection of the general blood-stream thereby. An infected limb may be dealt with by amputation above the seat of the lesion, or it may be feasible to dissect out the infected veins. When abscesses have formed they must be dealt with by opening and washing out the cavities. Antistreptococcic serum may be tried, as in septicaemia; and if there be time to prepare a vaccine it offers the best prospects, more particularly in the subacute and chronic forms of pyaemia. The usual administration of nourishing diet and stimulants when required should be undertaken, and every effort made to keep up the patient's strength.

REFERENCES. - Watson Cheyne in Clifford Albutt's System of Medicine (1906); Horder in the Practitioner (May 1908); Spencer and Gask's System of Surgery (Iwo); Barr, Bell and Douglas, Lancet (Feb. 1907); H. Jellett, Manual of Midwifery (1905); Whyte in Edinburgh Medical Journal (Dec. 1907); Sir A. Wright in the Lancet (Nov. 1907); Whitridge Williams in American Journal of Obstetrics (May 1909); R. Park, The Principles of Surgery (1908); George Taylor in the Practitioner (March 1910). (H. L. H.)


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Simple English

A Sepsis is a very dangerous disease. It occurs when an infection goes wrong. The pathogen was at some point able to get into the blood or tissues.[1] The term sepsis is frequently used to refer to septicemia (blood poisoning). Septicemia is only one type of sepsis.[1][2] Bacteremia specifically refers to the presence of bacteria in the bloodstream (viremia and fungemia are the terms used for viruses and fungi).

Contents

Symptoms

Common symptoms of sepsis are inflammations all over the body. This is often combined with high fever. Today, people believe, these symptoms are caused by the immune system trying to fight the disease. Because of the strong reactions, organs can be damaged in the process.

Cause of death

In the United States, sepsis is the leading cause of death for ICU patients which do not have heart problems. Data from the Centers for Disease Control and Prevention shows it is the tenth most common cause of death overall.[3] Older people, those with a weak immune system and those with a strong illness suffer from sepis more often. It is also more dangerous to them. It occurs in 1%-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 over 60% for septic shock.

More severe forms

Severe sepsis and septic shock are more severe forms of sepis. With severe sepsis, one or more organs fail to work. Septic shock is when sepis is combined with very low blood pressure

Treatment

Today, the bacterial forms of sepsis can be treated with antibiotics. In addition, the bad fluids (blood) have to be replaced. It might also necessary to functionally replace the organs that failed.

About half the people affected die from the condition. Rapid access to treatment will increase the chances of survival, in most cases.

References

  1. 1.0 1.1 "Sepsis". eMedicine Online Medical Dictionary. http://www.emedicine.com/asp/dictionary.asp?keyword=sepsis. Retrieved 2008-02-22. 
  2. "Septicemia". eMedicine Online Medical Dictionary. http://www.emedicine.com/asp/dictionary.asp?keyword=septicemia. Retrieved 2007-06-30. 
  3. Martin GS, Mannino DM, Eaton S, Moss M (2003-04-17). "The epidemiology of sepsis in the United States from 1979 through 2000". N Engl J Med 348 (16): 1546-54. PMID 12700374. http://content.nejm.org/cgi/content/full/348/16/1546. 

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