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Therapeutic approaches to reduce systemic inflammation in septic-associated neurologic complications

Published online by Cambridge University Press:  01 February 2008

M. L. Wratten
M. L. Wratten*
Affiliation:
Sorin Group, Acute Therapies, Mirandola (MO), Italy
*
Correspondence to: Mary Lou Wratten, Acute Therapies, Sorin Group, Via Camurana 1, 41037 Mirandola (MO), Italy. E-mail: marylou.wratten@sorin.com; Mobile: +39 335 7800209; Office Tel: +39 0535 29281; Fax: +39 0535 29282
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Summary

Treatment of severe sepsis and septic shock often focuses on resolving immediate life-threatening problems related to infection (source control, antibiotics) and providing circulatory, ventilatory and other organ support. Neurologic complications, such as sepsis-associated encephalopathy, frequently occur in septic patients and are associated with higher mortality and long-term complications. As case fatalities and overall mortality continue to decline, long-term cognitive problems are becoming more common among survivors. Although the aetiology of septic encephalopathy has not been clearly established, systemic inflammation appears to play a key role in altering both the blood–brain barrier permeability and amplifying the inflammatory response. Several new therapies are now aimed at reducing systemic inflammation. These may eventually play a role in reducing neurologic complications related to the acute pathophysiology of sepsis and may be able to reduce early cerebral dysfunction with the goal of reducing long-term neurologic complications. Coupled plasma filtration adsorption is an extracorporeal therapy aimed at the non-specific removal of cytokines and mediators involved in systemic inflammation and immune suppression by the use of plasma filtration coupled to an adsorbent resin cartridge with high affinity for many cytokines and mediators. Several cytokines that are removed by coupled plasma filtration adsorption have also been implicated in blood–brain barrier permeability, leucocyte recruitment and amplification of the inflammatory response. Current studies are ongoing to determine whether treatments such as coupled plasma filtration adsorption may also be beneficial in reducing long-term neurologic complications.

Keywords

SEPSISCYTOKINESENCEPHALOPATHYFILTRATION, plasma
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 25 , Issue S42 , February 2008 , pp. 1 - 7
Copyright
Copyright © European Society of Anaesthesiology 2008

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References

1.Dombrowskiy, V, Martin, A, Sunderram, J, Paz, H. Rapid increase in hospitalization and mortality rates for severe sepsis in the United States: a trend analysis from 1993 to 2003. Crit Care Med 2007; 35: 1244–1245.CrossRefGoogle Scholar
2.Angus, DC, Linde-Zwirble, WT, Lidicker, J, Clermont, G, Carcillo, J, Pinsky, MR. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001; 29: 1303–1310.CrossRefGoogle ScholarPubMed
3.Hotchkiss, RS, Karl, IE. The pathophysiology and treatment of sepsis. N Engl J Med 2003; 348: 138–150.CrossRefGoogle ScholarPubMed
4.Russell, JA. Management of sepsis. N Engl J Med 2006; 355: 1699–1713.CrossRefGoogle ScholarPubMed
5.Riedemann, NC, Guo, RF, Ward, PA. The enigma of sepsis. J Clin Invest 2003; 112: 460–467.CrossRefGoogle ScholarPubMed
6.Ronco, C, Tetta, C, Mariano, F et al. . Interpreting the mechanisms of continuous renal replacement therapy in sepsis: the peak concentration hypothesis. Artif Organs 2003; 27: 792–801.CrossRefGoogle ScholarPubMed
7.Imai, Y, Parodo, J, Kajikawa, O et al. . Injurious mechanical ventilation and end-organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome. JAMA 2003; 289: 2104–2112.CrossRefGoogle Scholar
8.Munford, R, Pugin, J. Normal responses to injury prevent systemic inflammation and can be immunosuppressive. Am J Respir Crit Care Med 2001; 163: 316–321.CrossRefGoogle ScholarPubMed
9.Consales, G, De Gaudio, AR. Sepsis associated encephalopathy. Minerva Anestesiol 2005; 71: 39–52.Google ScholarPubMed
10.Sharshar, T, Hopkinson, NS, Orlikowski, D, Annane, D. Science review: The brain in sepsis – culprit and victim. Crit Care 2005; 9: 37–44.CrossRefGoogle ScholarPubMed
11.Wilson, JX, Young, GB. Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts. Can J Neurol Sci 2003; 30: 98–105.CrossRefGoogle ScholarPubMed
12.Bolton, CF, Young, GB, Zochodne, DW. The neurological complications of sepsis. Ann Neurol 1993; 33: 94–100.CrossRefGoogle ScholarPubMed
13.Young, GB, Bolton, CF, Austin, TW, Archibald, YM, Gonder, J, Wells, GA. The encephalopathy associated with septic illness. Clin Invest Med 1990; 13: 297–304.Google ScholarPubMed
14.Papadopoulos, MC, Davies, DC, Moss, RF, Tighe, D, Bennett, ED. Pathophysiology of septic encephalopathy: a review. Crit Care Med 2000; 28: 3019–3024.CrossRefGoogle ScholarPubMed
15.Kastenbauer, S, Pfister, HW. Pneumococcal meningitis in adults: spectrum of complications and prognostic factors in a series of 87 cases. Brain 2003; 126: 1015–1025.CrossRefGoogle Scholar
16.Barlas, I, Oropello, JM, Benjamin, E. Neurologic complications in intensive care. Curr Opin Crit Care 2001; 7: 68–73.CrossRefGoogle ScholarPubMed
17.Sprung, CL, Peduzzi, PN, Shatney, CH et al. . Impact of encephalopathy on mortality in the sepsis syndrome. The Veterans Administration Systemic Sepsis Cooperative Study Group. Crit Care Med 1990; 18: 801–806.CrossRefGoogle ScholarPubMed
18.Young, GB, Bolton, CF, Archibald, YM, Austin, TW, Wells, GA. The electroencephalogram in sepsis-associated encephalopathy. J Clin Neurophysiol 1992; 9: 145–152.CrossRefGoogle ScholarPubMed
19.Nguyen, DN, Spapen, H, Su, F et al. . Elevated serum levels of S-100beta protein and neuron-specific enolase are associated with brain injury in patients with severe sepsis and septic shock. Crit Care Med 2006; 34: 1967–1974.CrossRefGoogle ScholarPubMed
20.Stocchetti, N. Brain and sepsis: functional impairment, structural damage, and markers. Anesth Analg 2005; 101: 1463–1464.CrossRefGoogle ScholarPubMed
21.Davies, DC. Blood–brain barrier breakdown in septic encephalopathy and brain tumours. J Anat 2002; 200: 639–646.CrossRefGoogle ScholarPubMed
22.du Moulin, GC, Paterson, D, Hedley-Whyte, J, Broitman, SA. E. coli peritonitis and bacteremia cause increased blood–brain barrier permeability. Brain Res 1985; 340: 261–268.CrossRefGoogle ScholarPubMed
23.Papadopoulos, MC, Lamb, FJ, Moss, RF, Davies, DC, Tighe, D, Bennett, ED. Faecal peritonitis causes oedema and neuronal injury in pig cerebral cortex. Clin Sci (Lond) 1999; 96: 461–466.CrossRefGoogle ScholarPubMed
24.Nassif, X, Bourdoulous, S, Eugene, E, Couraud, PO. How do extracellular pathogens cross the blood–brain barrier? Trends Microbiol 2002; 10: 227–232.CrossRefGoogle ScholarPubMed
25.Estrada, RV, Moreno, J, Martinez, E, Hernandez, MC, Gilsanz, G, Gilsanz, V. Pancreatic encephalopathy. Acta Neurol Scand 1979; 59: 135–139.CrossRefGoogle ScholarPubMed
26.Sharshar, T, Annane, D, de la Grandmaison, GL, Brouland, JP, Hopkinson, NS, Francoise, G. The neuropathology of septic shock. Brain Pathol 2004; 14: 21–33.CrossRefGoogle ScholarPubMed
27.Moss, R, Parmar, N, Tighe, D, Davies, D. Adrenergic agents modify cerebral edema and microvessel ultrastructure in porcine sepsis. Crit Care Med 2004; 32: 1916–1921.CrossRefGoogle ScholarPubMed
28.Hinkelbein, J, Schroeck, H, Peterka, A, Schubert, C, Kuschinsky, W, Kalenka, A. Local cerebral blood flow is preserved in sepsis. Curr Neurovasc Res 2007; 4: 39–47.CrossRefGoogle ScholarPubMed
29.Rosengarten, B, Hecht, M, Auch, D et al. . Microcirculatory dysfunction in the brain precedes changes in evoked potentials in endotoxin-induced sepsis syndrome in rats. Cerebrovasc Dis 2007; 23: 140–147.CrossRefGoogle ScholarPubMed
30.Cojocaru, IM, Musuroi, C, Iacob, S, Cojocaru, M. Investigation of TNF-alpha, IL-6, IL-8 and of procalcitonin in patients with neurologic complications in sepsis. Rom J Intern Med 2003; 41: 83–93.Google ScholarPubMed
31.Paul, R, Koedel, U, Winkler, F et al. . Lack of IL-6 augments inflammatory response but decreases vascular permeability in bacterial meningitis. Brain 2003; 126: 1873–1882.CrossRefGoogle ScholarPubMed
32.Rupprecht, TA, Angele, B, Klein, M et al. . Complement C1q and C3 are critical for the innate immune response to Streptococcus pneumoniae in the central nervous system. J Immunol 2007; 178: 1861–1869.CrossRefGoogle ScholarPubMed
33.Swiergiel, AH, Dunn, AJ. Effects of interleukin-1beta and lipopolysaccharide on behavior of mice in the elevated plus-maze and open field tests. Pharmacol Biochem Behav 2007; 86: 651–659.CrossRefGoogle ScholarPubMed
34.Dunn, AJ, Swiergiel, AH. The role of cytokines in infection-related behavior. Ann NY Acad Sci 1998; 840: 577–585.CrossRefGoogle ScholarPubMed
35.Krueger, JM, Walter, J, Dinarello, CA, Wolff, SM, Chedid, L. Sleep-promoting effects of endogenous pyrogen (interleukin-1). Am J Physiol 1984; 246: R994–R999.Google ScholarPubMed
36.Dantzer, R. Cytokine-induced sickness behavior: mechanisms and implications. Ann NY Acad Sci 2001; 933: 222–234.CrossRefGoogle ScholarPubMed
37.Serantes, R, Arnalich, F, Figueroa, M et al. . Interleukin-1beta enhances GABAA receptor cell-surface expression by a phosphatidylinositol 3-kinase/Akt pathway: relevance to sepsis-associated encephalopathy. J Biol Chem 2006; 281: 14632–14643.CrossRefGoogle ScholarPubMed
38.Moller, K, Strauss, GI, Qvist, J et al. . Cerebral blood flow and oxidative metabolism during human endotoxemia. J Cereb Blood Flow Metab 2002; 22: 1262–1270.CrossRefGoogle ScholarPubMed
39.Tsao, N, Hsu, HP, Wu, CM, Liu, CC, Lei, HY. Tumour necrosis factor-alpha causes an increase in blood–brain barrier permeability during sepsis. J Med Microbiol 2001; 50: 812–821.CrossRefGoogle ScholarPubMed
40.Bouman, CS, Oudemans-van Straaten, HM, Schultz, MJ, Vroom, MB. Hemofiltration in sepsis and systemic inflammatory response syndrome: the role of dosing and timing. J Crit Care 2007; 22: 1–12.CrossRefGoogle ScholarPubMed
41.Muirhead, E, Reid, A. Resin Artificial Kidney. J Lab Clin Med 1948; 33: 841–844.Google ScholarPubMed
42.Winchester, JF, Silberzweig, J, Ronco, C et al. . Sorbents in acute renal failure and endstage renal disease: middle molecule and cytokine removal. Blood Purif 2004; 22: 73–77.CrossRefGoogle ScholarPubMed
43.Howell, CA, Sandeman, SR, Phillips, GJ et al. . The in vitro adsorption of cytokines by polymer-pyrolysed carbon. Biomaterials 2006; 27: 5286–5291.CrossRefGoogle ScholarPubMed
44.Ronco, C, Brendolan, A, d’Intini, V, Ricci, Z, Wratten, ML, Bellomo, R. Coupled plasma filtration adsorption: rationale, technical development and early clinical experience. Blood Purif 2003; 21: 409–416.CrossRefGoogle ScholarPubMed
45.Ronco, C, Brendolan, A, Lonnemann, G et al. . A pilot study of coupled plasma filtration with adsorption in septic shock. Crit Care Med 2002; 30: 1250–1255.CrossRefGoogle ScholarPubMed
46.Mariano, F, Tetta, C, Stella, M, Biolino, P, Miletto, A, Triolo, G. Regional citrate anticoagulation in critically ill patients treated with plasma filtration and adsorption. Blood Purif 2004; 22: 313–319.CrossRefGoogle ScholarPubMed
47.Formica, M, Olivieri, C, Livigni, S et al. . Hemodynamic response to coupled plasma filtration-adsorption in human septic shock. Intensive Care Med 2003; 29: 703–708.CrossRefGoogle Scholar