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SEPSIS NETWORKING

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Sepsis is a potentially serious complication, the outcome of which, like other diseases, is influenced by the timeliness of diagnosis and appropriateness of therapy.
Severe sepsis and septic shock are major and costly health problems, affecting millions of people every year all over the world, whose incidence is on the increase and that mortality sometimes exceeds 25%.

SEPSI1

The initial management of sepsis does not require the use of diagnostic techniques, complex measures, or expensive medications or, in general, difficult to availability. Vice versa, if it is not promptly recognised and correctly managed in the early stages of onset, sepsis evolves into clinical forms that require health interventions that expensive and have a high mortality. For these reasons, today, sepsis is among the health issues most relevant to professionals, the health management and institutions.
Different conditions, however, hinder a significant improvement in mortality in our hospitals: lack of awareness of the size of the problem, lack of knowledge and skills, poor attitude to work in team, lack of paths, organizational, resources are not always widely available.
The project to improve sepsis management in Health care organizations in the Province of Catania was founded by one of the objectives of the Plan for the Implementation of the Inter-company, and is aimed at the promotion of a new culture of care and organisation, the definition and dissemination of a series of good practice based on evidence, of a path of implementation and dissemination of the same and monitoring the level of membership, as well as to the creation of a network that allows you to share knowledge and resources.
The goal is ambitious: to reduce the mortality in cases of sepsis, severe and septic shock.
In general, the actions that the project intends to pursue are:

  • recognize early cases of sepsis;
  • immediately initiate the procedures diagnostic and therapeutic most appropriate;
  • promote a path of organizational management of the patient with sepsis in order to ensure a setting of care appropriate;
  • schedule a task training for the professionals of the disciplines involved in the management of sepsis;
  • plan activities, implementation of the best practices identified;
  • plan an activity for the periodic monitoring by the audit dedicated, aimed at verifying the level of adherence to the good practices proposed, and a measure of the output of the process and the outcomes.
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I TOP TEN

I TOP TEN

I TOP TEN

I TOP TEN

The top ten in the management of sepsis

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7

1

Identify sepsis

The term sepsis is a syndrome characterized by “organ dysfunction life-threatening sustained by an altered host response to the infection.”
This new definition emphasizes the primacy of the host response to infection, and the potential for lethality that is significantly above of an infection straightforward and the need for a timely recognition.
The organ dysfunction can be defined as an acute change in the total score (SOFA ≥2 due to the infection.
In patients not known to have organ dysfunction pre-existing, the score for the SOFA base can be assumed to be equal to zero.
At-risk patients, with suspected infection, can be be readily identified with the qSOFA, that is, with the evaluation of altered mental status, systolic blood pressure and respiratory rate.[1]
The emphasis on organ dysfunction life-threatening e-mail in the definition of “The Third International Consensus Definitions for Sepsis and Septic Shock”[1] is that the term "severe sepsis" would be unnecessary.
The same document defines septic shock as a subset of sepsis in which the circulatory abnormalities, and cellular metabolic are so serious as to substantially increase the mortality.[1]
Patients with septic shock can be identified as patients with sepsis with persistent hypotension requiring vasopressors to maintain PAM ≥65 mm Hg, and having levels, and serum lactates > 2 mmol / L (18 mg/dL) despite unadeguato intake of fluids.[1]
However, the new definitions of sepsis and of septic shock, reflecting the advances in the pathophysiology and sepsis, and provide greater specificity in describing the life-threatening conditions do not change the primary objective of early identification of sepsis and timely initiation of treatment in the management of this population of vulnerable patients”.[2]

 

[1] Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA 2016;315:801-10

[2] http://www.survivingsepsis.org/SiteCollectionDocuments/SSC-Statements-Sepsis-Definitions-3-2016.pdf

sepsi2

A militant application of these criteria and divorced from the clinical context of the individual patient, can be misleading.


The evaluation of vital parameters and laboratory tests should be interpreted with caution, setting them to the clinical history and condition of the patient.
 

2

Monitoring of vital parameters (PA, Fc, HGT, SpO2, Tc, urine output)

All patients with a diagnosis of sepsis should be subjected to the monitoring of vital parameters.

 

The monitoring of vital parameters should be recorded in the health records.
 

3

Measurement of the blood concentration of lactates

High levels of lactates are the expression of the hypoperfusion to the tissue.
The measurement of the plasma concentration of lactates is essential not only for the diagnosis of sepsis, severe, but also to monitor the effectiveness of the infusion administration in cases of septic shock.
In fact, in patients with lactates ≥ 2 mmol/L, the goal of treatment is to normalize the levels of lactates.
The measurement of the plasma concentration of lactates is a marker accurate hypoperfusion of tissue, providing an alternative diagnostic effective saturation, central venous oxygen (ScvO2).
In addition, the plasma concentration of lactates is an important prognostic factor. Patients with sepsis severe or septic shock who do not have a reduction in > 10% of lactates (clearance of the lactates) within 6 hours, show a significant increase of mortality.[3-13]
 

[3] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012

[4] Rivers EP, Yataco AC, Jaehne AK, Gill J, Disselkamp, M. Oxygen extraction and perfusion markers in severe sepsis and septic shock: diagnostic, therapeutic and outcome implications. Curr Opin Crit Care. 2015 Oct;21(5):381-7.

[5] Silva Ramos FJ, Azevedo LC. Hemodynamic and perfusion end points for volemic resuscitation in sepsis. Shock. 2010 Sep;34 Suppl 1:34-9.

[6] Permpikul C, Cheranakhorn C. The temporal changes of tissue oxygen saturation (StO2) and central venous oxygen saturation (ScvO2) during sepsis/septic shock resuscitation. J Med Assoc Thai. 2014 Mar;97 Suppl 3:S168-75.

[7] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012

[8] Jones AE, Shapiro NI, Trzeciak S, Arnold RC, Claremont HA, Kline JA Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA. 2010 Feb 24;303(8):739-46.

[8] Yu B, Tian HY, Hu ZJ, et al. Comparison of the effect of fluid resuscitation as guided either by the lactate clearance rate, or by central venous oxygen saturation in patients with sepsis. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2013 Oct;25(10):578-83.

[10] Levy MM, Dellinger RP, Townsend SR, et al. Surviving Sepsis Campaign: The Surviving Sepsis Campaign: Results of an international guideline-based performance improvement program targeting severe sepsis. Crit Care Med 2010; 38:367-374

[11] Levy MM, Rhodes A, Phillips GS, Townsend SR, et al. Surviving Sepsis Campaign: association between performance metrics and outcomes in a 7.5-year study. Crit Care Med. 2015 Jan;43(1):3-12.

[12] Kruse O1, belgië ministère de la communauté N, Barfod C. Blood lactate as a predictor for in-hospital mortality in patients admitted acutely to hospital: a systematic review. Scand J Trauma Resusc Emerg Med. 2011 Dec 28;19:74.

[13] Nguyen HB1, Rivers EP, Knoblich BP, Jacobsen G, Muzzin A, Ressler JA, Tomlanovich MC. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med. 2004 Aug;32(8):1637-42.

4

Monitoring of the baroreceptor

There is a widespread consensus in the literature that the monitoring of the central venous pressure (PVC) and saturation central venous oxygen (ScvO2) are needed to measure the achievement of therapeutic goals.
However, it is not always possible to perform the monitoring of the central venous pressure (PVC) and saturation central venous oxygen (ScvO2).
The measurement of the caliber of the inferior vena cava and the diameter of the right ventricle by ultrasound examination, are the methods equivalent to evaluate the baroreceptor, which was not invasive.[14-18]

 

[14] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
[15] Levy MM, Dellinger RP, Townsend SR, et al. Surviving Sepsis Campaign: The Surviving Sepsis Campaign: Results of an international guideline-based performance improvement program targeting severe sepsis. Crit Care Med 2010; 38:367-374
[16] Zengin S, Al B, Genc S, et al. Role of inferior vena cava and right ventricular diameter in assessment of volume status: a comparative study: ultrasound and hypovolemia. Am J Emerg Med. 2013 May;31(5):763-7.
[17] Lee CW, Kory PD, Arntfield RT. Development of a fluid resuscitation protocol using inferior vena cava, and lung ultrasound. J Crit Care. 2016 Feb;31(1):96-100.
[18] Deshpande R, Akhtar S, Haddadin AS. Utility of ultrasound in the ICU. Curr Opin Anaesthesiol. 2014 Apr;27(2):123-32.

5

Running samples for blood culture from peripheral vein and/or from a CVC if it is inserted > 48 hours

Before starting the antibiotic therapy, it is necessary to perform cultures appropriate, if this does not cause a significant delay (>45 minutes) at the beginning of the administration of antimicrobials. To optimize the identification of micro-organisms, you must perform at least two groups of blood cultures: one by means of venipuncture (for aerobes, anaerobes and fungi) and one through each device of the vascular access, unless the device has been inserted recently (<48 hours). Cultures from other sites, such as urine, cerebrospinal fluid, wounds, respiratory secretions or other body fluids that may be the source of infection, should be performed before antimicrobial therapy if doing so does not cause a significant delay in administration of antibiotics.
Obtaining blood cultures peripherally and through a device of the vascular access is an important strategy. If you isolated the same organism from both cultures, the likelihood that the organism you are causing the sepsis is highest.
There is consensus on the fact that molecular techniques may have an important role in reducing the time of diagnosis compared to traditional crops. The decrease in turnaround time can reduce the use of treatments which are inappropriate, unwanted side effects, as well as the induction of resistant strains. In the final analysis, a rapid diagnosis improves the stewardship antimicrobial, but especially the outcome.[19-22]

 

[19] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012

[20] Mongelli G et al J. Med Microbiol 2015; 64(7): 270Kollef MH et al Chest 1999; 115: 462

[21] Kumar A et al Crit Care med 2006; 34: 1589

[22] Schermann Ge et al Crit Care Med 2006; 34: 2069
 

6

Imaging study for the possible location of the loci of infectious

It is recommended to run readily to imaging studies in an attempt to confirm a potential source of infection.
The potential sources of infection should be sampled if identified, considering the risks to the patient associated with the transport and execution of invasive procedures.
[23]

 

[23] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012

7

Running the assay procalcitonin and beta-glucan

Procalcitonin
The utility of the levels of procalcitonin or other biomarkers (such as C-reactive protein) to discriminate the acute inflammatory response of sepsis from other causes of generalized inflammation is not contradictory and should be reported to the clinical context and setting of care.
In fact, while there are no recommendations for the use of these markers to distinguish between severe infection and other acute inflammatory states, such as, for example, the post-operative or other forms of shock, - - - in other contexts, such as, for example, in the context of the initial assessment in the critical area, the dosage of procalcitonin provides a significant contribution, in the context of the clinical context of the individual patient, to identify cases of sepsis and cases that require timely administration of antibiotics.[24-29]

 

 

 

 

 

 

 

 

 

 

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Betaglucan

The dosage of beta-glucan and/or mannan and anti-mannan, are indicated in the differential diagnosis between infections etiology bacterial infections etiology fungal.
However, the dosage of beta-glucan and/or mannan and anti-mannan has a high false positive rate, while the method has a negative predictive value.[30]

[24] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
[25] Giamarellos-Bourboulis EJ, Giannopoulou P, Grecka P, et al: Should procalcitonin be introduced in the diagnostic criteria for the systemic inflammatory response syndrome and sepsis? J Crit Care 2004;19:152-157.
[26] Uzzan B, Cohen R, Nicolas P, et al: Procalcitonin as a diagnostic test for sepsis in critically ill adults and after surgery or trauma: A systematic review and meta-analysis. Crit Care Med 2006; 34:1996-2003.
[27] Tang BM, Eslick GD, Craig JC, et al: Accuracy of procalcitonin for sepsis diagnosis in critically ill patients: Systematic review and metaanalysis. Lancet Infect Dis 2007; 7:210-217.

[28] Bouadma L, Luyt CE, Tubach et al. The. PRORATA trial group. Use of procalcitonin to reduce patients' exposure to antibiotics in intensive care units (PRORATA trial): a multicentre randomised controlled trial. Lancet. 2010 Feb 6;375(9713):463-74.
[29] Prkno A, Wacker C, Brunkhorst FM, Schlattmann P. Procalcitonin-guided therapy in intensive care unit patients with severe sepsis and septic shock--a systematic review and meta-analysis. Crit Care. 2013 Dec 11;17(6):R291.

[30] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012

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8

Administration of antibiotic therapy

Intravenous administration of effective antimicrobials within the first hour of recognition of septic shock and sepsis severe without septic shock, it should be the goal of therapy.[30]

 

[31] Guidet B, Martinet O, Boulain T, et al. Assessment of hemodynamic efficacy and safety of 6% hydroxyethylstarch 130/0.4 vs. 0.9% NaCl fluid replacement in patients with severe sepsis: the CRYSTMAS study. Crit Care. 2012 May 24;16(3):R94.

9

Administration of therapy with crystalloid for hypotension persisted or in the case of Lactates >4mmol/L

Un trattamento iniziale inadeguato e il ritardo nella stabilizzazione emodinamica possono essere associati ad un aumentato rischio di morte nei pazienti con sepsi grave.  
L’utilizzo degli amidi idrossietilici e dell’albumina è controverso. 
I cristalloidi sono i liquidi di scelta nel trattamento iniziale della sepsi grave e dello shock settico.[32-44]  

 

[32] Guidet B, Martinet O, Boulain T, et al. Assessment of hemodynamic efficacy and safety of 6% hydroxyethylstarch 130/0.4 vs. 0.9% NaCl fluid replacement in patients with severe sepsis: the CRYSTMAS study. Crit Care. 2012 May 24;16(3):R94.
[33] Brunkhorst FM, Engel C, Bloos F, et al; German Competence Network Sepsis (SepNet): Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med 2008; 358:125–139
[34] Guidet B, Martinet O, Boulain T, et al: Assessment of hemodynamic efficacy and safety of 6% hydroxyethylstarch 130/0.4 vs. 0.9% NaCl fluid replacement in patients with severe sepsis: The CRYSTMAS study. Crit Care 2012; 16:R94
[35] Perner A, Haase N, Guttormsen AB, et al; 6S Trial Group; Scandinavian Critical Care Trials Group: Hydroxyethyl starch 130/0.42 versus Ringer’s acetate in severe sepsis. N Engl J Med 2012; 367:124–134

[36 ]Myburgh JA, Finfer S, Bellomo R, et al; CHEST Investigators; Australian and New Zealand Intensive Care Society Clinical Trials Group: Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med 2012; 367:1901–1911

[37] Perel P, Roberts I: Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2011; 3: CD000567
[38] Schortgen F, Lacherade JC, Bruneel F, et al: Effects of hydroxyethylstarch and gelatin on renal function in severe sepsis: A multicenter randomised study. Lancet 2001; 357:911–916

[39] McIntyre LA, Fergusson D, Cook DJ, et al; Canadian Critical Care Trials Group: Fluid resuscitation in the management of early septic shock (FINESS): A randomized controlled feasibility trial. Can J Anaesth 2008; 55:819–826
[40] Brunkhorst FM, Engel C, Bloos F, et al; German Competence Network Sepsis (SepNet): Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med 2008; 358:125–139
[41 ]Finfer S, Bellomo R, Boyce N, et al; SAFE Study Investigators: A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350:2247–2256
[42] Delaney AP, Dan A, McCaffrey J, et al: The role of albumin as a resuscitation fluid for patients with sepsis: A systematic review and metaanalysis. Crit Care Med 2011; 39:386–391
[43] Mutter TC1, Ruth CA, Dart AB. Hydroxyethyl starch (HES) versus other fluid therapies: effects on kidney function. Cochrane Database Syst Rev. 2013 Jul 23;7:CD007594. doi: 10.1002/14651858.CD007594.pub3.
[44] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012

10

Administration of therapy with vasopressors, inotropes, and/or corticosteroids in case of hypotension, persistent

Vasopressors
In patients with septic shock, when the administration of fluids fails to restore adequate blood pressure and adequate perfusion, therapy should be initiated with medications vasopressors. The ultimate goals of such therapy in shock are to restore effective tissue perfusion and normalize cellular metabolism.
The initial treatment with vasopressors in order to obtain a mean arterial pressure of 65 mmHg.
The drug of choice is norepinephrine.
Epinephrine (added to and potentially substituted norepinephrine) is indicated when you need an additional drug to maintain an adequate blood pressure.
Some studies suggest that epinephrine has a negative effect on the circulation splancnica and produces hyperlactatemia. No clinical evidence shows, however, that epinephrine produces outcomes unfavorable, and should be the first alternative to norepinephrine.
With its effects alpha-adrenergic almost pure, the phenylephrine is the agent adrenergic that is less likely to produce tachycardia, but it may decrease stroke volume and is therefore not recommended in the treatment of septic shock except in circumstances where:
(a) are associated with serious arrhythmias, or
b) the cardiac output is high, or
(c) as salvage therapy when other vasopressors have failed to achieve the goal of a systolic blood pressure an average of 65 mmHg.
The vasopressin, with 0.03 units / minute can be added to norepinephrine (NE) with the intent of increasing both the mean arterial blood pressure, or reduce the amount of norepinephrine administered.
In septic shock, the levels of vasopressin are lower than those envisaged for a state of shock, especially in the stage subsequent to the initial one.
Low doses of vasopressin may be effective in raising blood pressure in patients refractory to other vasopressors and may have other potential physiological benefits.
Terlipressin has similar effects but has a longer duration of action.
Low doses of vasopressin are not recommended as a single vasopressore initial treatment of hypotension induced by sepsis. Higher doses to 0.03-0.04 units / minute should be reserved to salvage therapy.
The dopamine as an agent vasopressore is an alternative to norepinephrine only in highly selected patients (e.g., patients at low risk of tachyarrhythmias and bradycardia relative or absolute). There is no evidence regarding the use of dopamine at low doses for the renal protection.
Inotropic agents
The dobutamine up to 20 micrograms / kg / min, can be administered or added to vasopressore (if in use) in the presence of:
(a) myocardial dysfunction in the presence of elevated cardiac filling pressures and low cardiac output, or
(b) in the presence of signs of hypoperfusion, despite achieving adequate intravascular volume and adequate mean systolic blood pressure.
Corticosteroids
In septic shock patients, an adequate reintegration of fluids and medications, vasopressors, does not require the use of corticosteroids.
In the event that an adequate re-integration of fluids and medications, vasopressors do not reach the therapeutic goal is possible to administer hydrocortisone intravenously at a dose of 200 mg per day.[45-80]

[45] Hollenberg SM. Inotrope and vasopressor therapy of septic shock. Crit Care Clin. 2009 Oct;25(4):781-802, ix. doi: 10.1016/j.ccc.2009.07.003..
[46] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
[47] Hollenberg SM, Ahrens TS, Annane D, et al: Practice parameters for hemodynamic support of sepsis in adult patients: 2004 update. Crit Care Med 2004; 32:1928-1948

[48] LeDoux D, alfredo astiz ME, Carpati CM, et al: Effects of perfusion pressure on tissue perfusion in septic shock. Crit Care Med 2000; 28:2729-2732

[49]Martin C, Papazian L, Perrin G, et al: Norepinephrine or dopamine for the treatment of hyperdynamic septic shock? Chest 1993; 103: 1826-1831
[50] Vasu TS, Cavallazzi R, Hirani A, et al. Norepinephrine or dopamine for septic shock: systematic review of randomized clinical trials. J Intensive Care Med. 2012 May-Jun;27(3):172-8. doi: 10.1177/0885066610396312. Epub 2011 Mar 24.
[51] Martin C, Viviand X, Leone M, et al. Effect of norepinephrine on the outcome of septic shock. Crit Care Med. 2000 Aug;28(8):2758-65.
[52] Pollard S, Edwin SB, Alaniz C. Vasopressor and Inotropic Management Of Patients With Septic Shock. P T. 2015 Jul;40(7):438-50.
[53] Levy B, Bollaert PE, Charpentier C, et al: Comparison of norepinephrine and dobutamine to epinephrine for hemodynamics, lactate metabolism, and gastric tonometric variables in septic shock: A prospective, randomized study. Intensive Care Med 1997; 23:282-287.
[54] Annane D, Vignon P, Renault A, et al; CATS Study Group: Norepinephrine plus dobutamine versus epinephrine alone for management of septic shock: A randomised trial. Lancet 2007; 370:676-684.
[55] Seguin P, Bellissant E, Le Tulzo Y, et al: Effects of epinephrine compared with the combination of dobutamine and norepinephrine on gastric perfusion in septic shock. Clin Pharmacol Ther 2002; 71:381-388.

[56] Myburgh JA, Higgins A, Jovanovska A, et al; CAT Study investigators: A comparison of epinephrine and norepinephrine in critically ill patients. Intensive Care Med 2008; 34:2226-2234.
[57] Havel C1, Arrich J, Losert H, Gamper G, Müllner M, Herkner H. Vasopressors for hypotensive shock. Cochrane Database Syst Rev. 2011 May 11;(5):CD003709. doi: 10.1002/14651858.CD003709.pub3.
[58] Morelli A, Ertmer C, Rehberg S, et al: Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: A randomized, controlled trial. Crit Care 2008; 12:R143
[59] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
[60] Landry DW, Levin HR, Gallant EM, et al: Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation 1997; 95:1122-1125
[61] vSharshar T, Blanchard A, Paillard M, et al. Circulating vasopressin levels in septic shock. Crit Care Med. 2003 Jun;31(6):1752-8.
[62] Russell JA. Bench-to-bedside review: Vasopressin in the management of septic shock. Crit Care. 2011 Aug 11;15(4):226.
[63] Patel BM, Chittock DR, Russell JA, et al: Beneficial effects of short term vasopressin infusion during severe septic shock. Anesthesiology 2002; 96:576-582.
[64] Dünser MW, Mayr AJ, Ulmer H, et al: Arginine vasopressin in advanced vasodilatory shock: A prospective, randomized, controlled study. Circulation 2003; 107:2313-2319
[65] Holmes CL, Patel BM, Russell JA, et al: Physiology of vasopressin relevant to management of septic shock. Chest 2001; 120:989-1002
[66] Malay MB, Ashton RC Jr, Landry DW, et al: Low-dose vasopressin in the treatment of vasodilatory septic shock. J Trauma 1999; 47:699-703; discussion 703
[67] Holmes CL, Walley KR, Chittock DR, et al: The effects of vasopressin on hemodynamics and renal function in severe septic shock: A case series. Intensive Care Med 2001; 27:1416-1421
[68] Lauzier F, Lévy B, Lamarre P, et al: Vasopressin or norepinephrine in early hyperdynamic septic shock: A randomized clinical trial. Intensive Care Med 2006; 32:1782-1789
[69] Serpa Neto A, Nassar AP, Cardoso SO, Manetta JA, Pereira VG, Espósito DC, Damasceno MC, Russell JA. Vasopressin and terlipressin in adult vasodilatory shock: a systematic review and meta-analysis of nine randomized controlled trials. Crit Care. 2012 Aug 14;16(4):R154.

[70] O'brien A, Clapp L, Singer M: Terlipressin for norepinephrine-resistant septic shock. Lancet 2002; 359:1209-1210
[71] Svoboda P, Scheer P, Kantorová I, Et al. Terlipressin in the treatment of late phase catecholamine-resistant septic shock Hepatogastroenterology. 2012 Jun;59(116):1043-7.
[72] Serpa Neto A, Nassar AP, Cardoso SO, et al. Vasopressin and terlipressin in adult vasodilatory shock: a systematic review and meta-analysis of nine randomized controlled trials. Crit Care. 2012 Aug 14;16(4):R154. doi: 10.1186/cc11469.
[73] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
[74] Bellomo R, Chapman M, Finfer S, et al: Low-dose dopamine in patients with early renal dysfunction: A placebo-controlled randomized trial. The Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet 2000; 356:2139-2143
[75] Kellum JA, M Decker J: Use of dopamine in acute renal failure: A meta-analysis. Crit Care Med 2001; 29:1526-1531
[76] Friedrich JO, Adhikari N, Herridge MS, et al. Meta-analysis: low-dose dopamine increases urine output but does not prevent renal dysfunction or death. Ann Intern Med. 2005 Apr 5;142(7):510-24.
[77] Gattinoni L, Brazzi L, Pelosi P, et al: A trial of goal-oriented hemodynamic therapy in critically ill patients. Svo2 Collaborative Group. N Engl J Med 1995; 333:1025-1032.
[78] Hayes MA, Timmins AC, Yau EH, et al: Elevation of systemic oxygen delivery in the treatment of critically ill patients. N Engl J Med 1994; 330:1717-1722.
[79] Nadeem R1, Sockanathan S, Singh M, ET AL. Impact of Dobutamine in Patients with Septic Shock: A Meta-Regression Analysis. Am J Ther. 2015 Jul 8.
[80] www.survivingsepsis.org/guidelines. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012


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