11/11/13

Distributive Shock

Today News Reference Education Log In Register

Distributive Shock
Author: Lalit K Kanaparthi, MD; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM more... Updated: Feb 12, 2013

Background
Distributive shock results from excessive vasodilation and the impaired distribution of blood flow. Septic shock is the most common form of distributive shock and is characterized by considerable mortality. In the United States, this is the leading cause of noncardiac death in intensive care units (ICUs). (See Pathophysiology, Etiology, Epidemiology, and Prognosis.) Other causes of distributive shock include systemic inflammatory response syndrome (SIRS) due to noninfectious inflammatory conditions such as burns and pancreatitis; toxic shock syndrome (TSS); anaphylaxis; reactions to drugs or toxins, including insect bites, transfusion reaction, and heavy metal poisoning; addisonian crisis; hepatic insufficiency; and neurogenic shock due to brain or spinal cord injury . (See Pathophysiology and Etiology.)

Types of shock
Shock is a clinical syndrome characterized by inadequate tissue perfusion that results in end-organ dysfunction. It can be divided into the following 4 categories: Distributive shock (vasodilation), which is a hyperdynamic process Cardiogenic shock (pump failure) Hypovolemic shock (intravascular volume loss) Obstructive shock (physical obstruction of blood circulation and inadequate blood oxygenation)

Systemic inflammatory response syndrome

The American College of Chest Physicians/Society of Critical Care Medicine (ACCP/SCCM) Consensus Conference Committee defined SIRS as the presence of at least 2 of the following 4 criteria (see Presentation)[1] : Core temperature of higher than 38C (100.0F) or lower than 36C (96.8F) Heart rate of more than 90 beats per minute Respiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO2) less than 32mm Hg White blood cell (WBC) count of more than 12,000/L, less than 4,000/L, or more than 10% immature (band) forms The clinical suspicion of systemic inflammatory response syndrome by an experienced clinician is also important.

Patient education
For patient education information, see Shock and Cardiopulmonary Resuscitation (CPR).

Pathophysiology
In distributive shock, the inadequate tissue perfusion is caused by loss of the normal responses of vascular
emedicine.medscape.com/article/168689-overview 1/8

11/11/13

Distributive Shock

smooth muscle to vasoconstrictive agents coupled with a direct vasodilating effect. The net result in a fluidresuscitated patient is a hyperdynamic, hypotensive state associated with increased mixed venous O2 saturation; however, evidence of tissue ischemia as manifest by an increased serum lactate, presumably due to intraorgan functional shunts. Early septic shock (warm or hyperdynamic) causes reduced diastolic blood; widened pulse pressure; flushed, warm extremities; and brisk capillary refill from peripheral vasodilation, with a compensatory increase in cardiac output. In late septic shock (cold or hypodynamic), myocardial contractility combines with peripheral vascular paralysis to induce a pressure-dependent reduction in organ perfusion. The result is hypoperfusion of critical organs such as the heart, brain, and liver. The hemodynamic derangements observed in septic shock and SIRS are due to a complicated cascade of inflammatory mediators. Inflammatory mediators are released in response to any of a number of factors, such as infection, inflammation, or tissue injury. For example, bacterial products such as endotoxin activate the host inflammatory response, leading to increased pro-inflammatory cytokines (eg, tumor necrosis factor (TNF), interleukin (IL)1b, and IL-6). Toll-like receptors are thought to play a critical role in responding to pathogens as well as in the excessive inflammatory response that characterizes distributive shock; these receptors are considered possible drug targets. Cytokines and phospholipid-derived mediators act synergistically to produce the complex alterations in vasculature (eg, increased microvascular permeability, impaired microvascular response to endogenous vasoconstrictors such as norepinephrine) and myocardial function (direct inhibition of myocyte function), which leads to maldistribution of blood flow and hypoxia. Hypoxia also induces the upregulation of enzymes that create nitric oxide, a potent vasodilator, thereby further exacerbating hypoperfusion. The coagulation cascade is also affected in septic shock. In septic shock, activated monocytes and endothelial cells are sources of tissue factor that activates the coagulation cascade; cytokines, such as IL-6, also play a role. The coagulation response is broadly disrupted, including impairment of antithrombin and fibrinolysis. Thrombin generated as part of the inflammatory response can trigger disseminated intravascular coagulation (DIC). DIC is found in 25-50% of patients with sepsis and is a significant risk factor for mortality.[2, 3] During distributive shock, patients are at risk for diverse organ system dysfunction that may progress to multiple organ failure (MOF). Mortality from severe sepsis increases markedly with the duration of sepsis and the number of organs failing. In distributive shock due to anaphylaxis, decreased SVR is due primarily to massive histamine release from mast cells after activation by antigen-bound immunoglobulin E (IgE), as well as increased synthesis and release of prostaglandins. Neurogenic shock is due to loss of sympathetic vascular tone from severe injury to the nervous system.

Etiology
The most common etiology of distributive shock is sepsis. Other causes include the following: SIRS due to noninfectious conditions such as pancreatitis, burns, or trauma TSS Anaphylaxis Adrenal insufficiency Reactions to drugs or toxins Heavy metal poisoning Hepatic insufficiency Neurogenic shock All of these conditions share the common characteristic of hypotension due to decreased SVR and low effective circulating plasma volume.

Septic shock
The most common sites of infection, in decreasing order of frequency, include the chest, abdomen, and genitourinary tract.

emedicine.medscape.com/article/168689-overview

2/8

11/11/13

Distributive Shock

Septic shock is commonly caused by bacteria, although viruses, fungi, and parasites are also implicated. Grampositive bacteria are being isolated more, with their numbers almost similar to those of gram-negative bacteria, which in the past were considered to be the predominant organisms. Multidrug-resistant organisms are increasingly common.[4]

Systemic inflammatory response syndrome

Causes of SIRS include the following: Infection Burns Surgery Trauma Pancreatitis Fulminant hepatic failure

Toxic shock syndrome

TSS can result from infection with Streptococcus pyogenes (group A Streptococcus ) or Staphylococcus aureus .

Adrenal insufficiency
Adrenal insufficiency can result from the following: Destruction of adrenal glands due to autoimmune disease, infection (tuberculosis, fungal infection, acquired immunodeficiency syndrome [AIDS]), hemorrhage, cancer, or surgical removal Suppression of hypothalamic-pituitary-adrenal axis by exogenous steroid, usually with doses at 20 mg daily or higher Hypopituitarism Metabolic failure in hormone production due to congenital conditions or drug-induced inhibition of synthetic enzymes (eg, metyrapone, ketoconazole)

Anaphylaxis
Anaphylaxis can develop as a result of the following: Drugs such as penicillins and cephalosporins Heterologous proteins such as Hymenoptera venom, foods, pollen, and blood serum products

Epidemiology
Occurrence in the United States
Sepsis develops in more than 750,000 patients per year in the United States. Angus and colleagues estimated that, by 2010, 1 million people per year would be diagnosed with sepsis.[5] From 1979-2000, the incidence of sepsis increased by 9% per year.

International occurrence
Sepsis is a common cause of death throughout the world and kills approximately 1,400 people worldwide every day.[6, 7]

Age-related demographics
Increased age correlates with increased risk of death from sepsis.

Prognosis
The mortality rate after development of septic shock is 20-80%.[8] Data suggest that mortality due to septic shock has decreased slightly because of new therapeutic interventions.[9] Early recognition and appropriate therapy are
emedicine.medscape.com/article/168689-overview 3/8

11/11/13

Distributive Shock

central to maximizing good outcomes. Identifying patients with septic shock in the emergency department, as opposed to identifying them outside of it, results in significantly improved mortality. In one study, the mortality rate for emergency department-identified patients was 27.7%, compared with 41.1% for patients identified outside of the emergency department.[10] Higher mortality rates have also been associated with the following: Advanced age The finding of positive blood cultures Infection with antibiotic-resistant organisms such as Pseudomonas aeruginosa Elevated serum lactate levels Impaired immune function Alcohol use Poor functional status prior to the onset of sepsis. Mortality rates associated with other forms of distributive shock are not well documented.

Complications
Duration of delirium is an independent predictor of long-term cognitive impairment. At 3-month and 12-month followup, as many as 79% and 71% of patients have cognitive impairment. About one third are severely impaired.[11, 12,
13]

Contributor Information and Disclosures

Author Lalit K Kanaparthi, MD Senior Fellow, Department of Pulmonary Medicine, Lenox Hill Hospital Lalit K Kanaparthi, MD is a member of the following medical societies: American College of Chest Physicians, American Medical Association, and American Thoracic Society Disclosure: Nothing to disclose. Coauthor(s) Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine Disclosure: Nothing to disclose. Ruben Peralta, MD, FACS Professor of Surgery, Anesthesia and Emergency Medicine, Senior Medical Advisor, Board of Directors, Program Chief of Trauma, Emergency and Critical Care, Consulting Staff, Professor Juan Bosch Trauma Hospital, Dominican Republic Ruben Peralta, MD, FACS is a member of the following medical societies: American Association of Blood Banks, American College of Healthcare Executives, American College of Surgeons, American Medical Association, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Massachusetts Medical Society, Society of Critical Care Medicine, and Society of Laparoendoscopic Surgeons Disclosure: Nothing to disclose. Chief Editor Michael R Pinsky, MD, CM, FCCP, FCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic
emedicine.medscape.com/article/168689-overview 4/8

11/11/13

Distributive Shock

Society, Association of University Anesthetists, European Society of Intensive Care Medicine, Shock Society, and Society of Critical Care Medicine Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting Additional Contributors Cory Franklin, MD Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science; Director, Division of Critical Care Medicine, Cook County Hospital Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences and Society of Critical Care Medicine Disclosure: Nothing to disclose. Sarah C Langenfeld, MD Assistant Professor, Department of Psychiatry, University of Massachusetts Medical School; Attending Psychiatrist, Community HealthLink Sarah Langenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Massachusetts Medical Society Disclosure: Nothing to disclose. Scott P Neeley, MD Medical Director, Intensive Care Unit, St Alexius Medical Center Scott P Neeley, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physician Executives, American College of Physicians, American Thoracic Society, Phi Beta Kappa, and Sigma Xi Disclosure: Nothing to disclose. Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment

References
1. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. Apr 2003;31(4):1250-6. [Medline]. 2. Vervloet MG, Thijs LG, Hack CE. Derangements of coagulation and fibrinolysis in critically ill patients with sepsis and septic shock. Semin Thromb Hemost. 1998;24(1):33-44. [Medline]. 3. Levi M. Pathogenesis and treatment of disseminated intravascular coagulation in the septic patient. J Crit Care. Dec 2001;16(4):167-77. [Medline]. 4. Friedman, Gilberto MD; Silva, Eliezer MD; Vincent, Jean-Louis MD, PhD, FCCM. Has the mortality of septic shock changed with time?. Critical Care Medicine. December 1998;26(12):2078-2086. [Full Text]. 5. 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. Jul 2001;29(7):1303-10. [Medline]. 6. Rubulotta FM, Ramsay G, Parker MM, Dellinger RP, Levy MM, Poeze M. An international survey: Public awareness and perception of sepsis. Crit Care Med. Jan 2009;37(1):167-70. [Medline].
emedicine.medscape.com/article/168689-overview 5/8

11/11/13

Distributive Shock

7. Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, et al. 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. Jun 1992;101(6):1644-55. [Medline]. 8. Parrillo JE. Pathogenetic mechanisms of septic shock. N Engl J Med. May 20 1993;328(20):1471-7. [Medline]. 9. Bernard GR, Vincent JL, Laterre PF, LaRosa SP, Dhainaut JF, Lopez-Rodriguez A, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med. Mar 8 2001;344(10):699-709. [Medline]. 10. Bastani A, Galens S, Rocchini A, Walch R, Shaqiri B, Palomba K, et al. ED identification of patients with severe sepsis/septic shock decreases mortality in a community hospital. Am J Emerg Med. Dec 26 2011;[Medline]. 11. Girard TD, Jackson JC, Pandharipande PP, et al. Delirium as a predictor of long-term cognitive impairment in survivors of critical illness. Crit Care Med. Jul 2010;38(7):1513-20. [Medline]. 12. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA. Apr 14 2004;291(14):1753-62. [Medline]. 13. Desai SV, Law TJ, Needham DM. Long-term complications of critical care. Crit Care Med. Feb 2011;39(2):371-9. [Medline]. 14. Marik PE, Kiminyo K, Zaloga GP. Adrenal insufficiency in critically ill patients with human immunodeficiency virus. Crit Care Med. Jun 2002;30(6):1267-73. [Medline]. 15. Sandham JD, Hull RD, Brant RF, et al. A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. N Engl J Med. Jan 2 2003;348(1):5-14. [Medline]. 16. Shah MR, Hasselblad V, Stevenson LW, Binanay C, O'Connor CM, Sopko G. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA. Oct 5 2005;294(13):1664-70. [Medline]. 17. Ince C. The microcirculation is the motor of sepsis. Crit Care. 2005;9 Suppl 4:S13-9. 18. Elbers PW, Ince C. Mechanisms of critical illness--classifying microcirculatory flow abnormalities in distributive shock. Crit Care. 2006;10(4):221. [Medline]. [Full Text]. 19. Micek ST, Roubinian N, Heuring T, et al. Before-after study of a standardized hospital order set for the management of septic shock. Crit Care Med. Nov 2006;34(11):2707-13. [Medline]. 20. Nguyen HB, Corbett SW, Steele R, et al. Implementation of a bundle of quality indicators for the early management of severe sepsis and septic shock is associated with decreased mortality. Crit Care Med. Apr 2007;35(4):1105-12. [Medline]. 21. Sebat F, Johnson D, Musthafa AA, et al. A multidisciplinary community hospital program for early and rapid resuscitation of shock in nontrauma patients. Chest. May 2005;127(5):1729-43. [Medline]. 22. Trzeciak S, Dellinger RP, Abate NL, et al. Translating research to clinical practice: a 1-year experience with implementing early goal-directed therapy for septic shock in the emergency department. Chest. Feb 2006;129(2):225-32. [Medline]. 23. Lagu T, Rothberg MB, Nathanson BH, Pekow PS, Steingrub JS, Lindenauer PK. Variation in the care of septic shock: The impact of patient and hospital characteristics. J Crit Care. Jan 31 2012;[Medline]. 24. Zambon M, Ceola M, Almeida-de-Castro R, Gullo A, Vincent JL. Implementation of the Surviving Sepsis Campaign guidelines for severe sepsis and septic shock: we could go faster. J Crit Care. Dec 2008;23(4):455-60. [Medline]. 25. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. Jun 2006;34(6):158996. [Medline]. 26. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and
emedicine.medscape.com/article/168689-overview 6/8

11/11/13

Distributive Shock

septic shock. N Engl J Med. Nov 8 2001;345(19):1368-77. [Medline]. 27. Jones AE, Focht A, Horton JM, Kline JA. Prospective external validation of the clinical effectiveness of an emergency department-based early goal-directed therapy protocol for severe sepsis and septic shock. Chest. Aug 2007;132(2):425-32. [Medline]. 28. Kortgen A, Niederprum P, Bauer M. Implementation of an evidence-based "standard operating procedure" and outcome in septic shock. Crit Care Med. Apr 2006;34(4):943-9. [Medline]. 29. McIntyre LA, Fergusson D, Cook DJ, et al. Resuscitating patients with early severe sepsis: a Canadian multicentre observational study. Can J Anaesth. Oct 2007;54(10):790-8. [Medline]. 30. McIntyre LA, Hebert PC, Fergusson D, Cook DJ, Aziz A. A survey of Canadian intensivists' resuscitation practices in early septic shock. Crit Care. 2007;11(4):R74. [Medline]. 31. Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med. Jan 2008;34(1):17-60. [Medline]. 32. Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med. Jan 2008;36(1):296-327. [Medline]. 33. Gunn SR, Fink MP, Wallace B. Equipment review: the success of early goal-directed therapy for septic shock prompts evaluation of current approaches for monitoring the adequacy of resuscitation. Crit Care. Aug 2005;9(4):349-59. [Medline]. 34. [Best Evidence] Dubois MJ, Orellana-Jimenez C, Melot C, et al. Albumin administration improves organ function in critically ill hypoalbuminemic patients: A prospective, randomized, controlled, pilot study. Crit Care Med. Oct 2006;34(10):2536-40. [Medline]. 35. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. May 27 2004;350(22):2247-56. [Medline]. 36. Finfer S, Bellomo R, McEvoy S, Lo SK, Myburgh J, Neal B, et al. Effect of baseline serum albumin concentration on outcome of resuscitation with albumin or saline in patients in intensive care units: analysis of data from the saline versus albumin fluid evaluation (SAFE) study. BMJ . Nov 18 2006;333(7577):1044. [Medline]. 37. Finfer S, Myburgh J, Bellomo R. Albumin supplementation and organ function. Crit Care Med. Mar 2007;35(3):987-8. [Medline]. 38. Myburgh J, Cooper DJ, Finfer S, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. Aug 30 2007;357(9):874-84. [Medline]. 39. Cavallaro F, Sandroni C, Marano C, La Torre G, Mannocci A, De Waure C, et al. Diagnostic accuracy of passive leg raising for prediction of fluid responsiveness in adults: systematic review and meta-analysis of clinical studies. Intensive Care Med. Sep 2010;36(9):1475-83. [Medline]. 40. Hassan M, Pham TN, Cuschieri J, Warner KJ, Nester T, Maier RV, et al. The association between the transfusion of older blood and outcomes after trauma. Shock . Jan 2011;35(1):3-8. [Medline]. 41. Zander R, Boldt J, Engelmann L, Mertzlufft F, Sirtl C, Stuttmann R. [The design of the VISEP trial. Critical appraisal]. Anaesthesist. Jan 2007;56(1):71-7. [Medline]. 42. [Best Evidence] Brunkhorst FM, Engel C, Bloos F, et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med. Jan 10 2008;358(2):125-39. [Medline]. 43. Holmes CL, Patel BM, Russell JA, Walley KR. Physiology of vasopressin relevant to management of septic shock. Chest. Sep 2001;120(3):989-1002. [Medline]. 44. Landry DW, Oliver JA. Vasopressin and relativity: on the matter of deficiency and sensitivity. Crit Care Med. Apr 2006;34(4):1275-7. [Medline]. 45. Lauzier F, Levy B, Lamarre P, Lesur O. Vasopressin or norepinephrine in early hyperdynamic septic shock: a randomized clinical trial. Intensive Care Med. Nov 2006;32(11):1782-9. [Medline].
emedicine.medscape.com/article/168689-overview 7/8

11/11/13

Distributive Shock

46. Russell JA, Walley KR, Singer J, et al. Vasopressin versus norepinephrine infusion in patients with septic shock. N Engl J Med. Feb 28 2008;358(9):877-87. [Medline]. 47. Serpa Neto A, Nassar Junior AP, Cardoso SO, Manettta JA, Pereira VG, Esposito DC, et al. Vasopressin and terlipressin in adult vasodilatory shock: a systematic review and meta-analysis of nine randomized controlled trials. Crit Care. Aug 14 2012;16(4):R154. [Medline]. 48. Holmes CL. Vasoactive drugs in the intensive care unit. Curr Opin Crit Care. Oct 2005;11(5):413-7. [Medline]. 49. Kinasewitz GT, Zein JG, Lee GL, et al. Prognostic value of a simple evolving disseminated intravascular coagulation score in patients with severe sepsis. Crit Care Med. Oct 2005;33(10):2214-21. 50. Zeerleder S, Hack CE, Wuillemin WA. Disseminated intravascular coagulation in sepsis. Chest. Oct 2005;128(4):2864-75. [Medline]. 51. Hoffmann JN, Vollmar B, Laschke MW, et al. Microcirculatory alterations in ischemia-reperfusion injury and sepsis: effects of activated protein C and thrombin inhibition. Crit Care. 2005;9 Suppl 4:S33-7. 52. Mackenzie AF. Activated protein C: do more survive?. Intensive Care Med. Dec 2005;31(12):1624-6. 53. O'Brien LA, Gupta A, Grinnell BW. Activated protein C and sepsis. Front Biosci. 2006;11:676-98. [Medline]. 54. Parrillo JE. Severe sepsis and therapy with activated protein C. N Engl J Med. Sep 29 2005;353(13):1398400. [Medline]. 55. Wiedermann CJ, Kaneider NC. A meta-analysis of controlled trials of recombinant human activated protein C therapy in patients with sepsis. BMC Emerg Med. Oct 14 2005;5:7. [Medline]. 56. Annane D, Bellissant E, Bollaert PE, Briegel J, Keh D, Kupfer Y. Corticosteroids for severe sepsis and septic shock: a systematic review and meta-analysis. BMJ . Aug 28 2004;329(7464):480. [Medline]. [Full Text]. 57. Raurich JM, Llompart-Pou JA, Ibanez J, et al. Low-dose steroid therapy does not affect hemodynamic response in septic shock patients. J Crit Care. Dec 2007;22(4):324-9. [Medline]. 58. [Best Evidence] Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med. Jan 10 2008;358(2):111-24. [Medline]. 59. Bruno JJ, Dee BM, Anderegg BA, Hernandez M, Pravinkumar SE. US practitioner opinions and prescribing practices regarding corticosteroid therapy for severe sepsis and septic shock. J Crit Care. Feb 14 2012;[Medline]. 60. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. Aug 21 2002;288(7):862-71. [Medline]. 61. [Best Evidence] Kinasewitz GT, Privalle CT, Imm A, et al. Multicenter, randomized, placebo-controlled study of the nitric oxide scavenger pyridoxalated hemoglobin polyoxyethylene in distributive shock. Crit Care Med. Jul 2008;36(7):1999-2007. [Medline]. 62. Jimenez MF, Marshall JC. Source control in the management of sepsis. Intensive Care Med. 2001;27 Suppl 1:S49-62. [Medline]. Medscape Reference 2011 WebMD, LLC

emedicine.medscape.com/article/168689-overview

8/8