Multiple Organ Dysfunction Syndrome in Sepsis Clinical Presentation
- Author: Ali H Al-Khafaji, MD, MPH; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more...
Symptoms of sepsis are usually nonspecific and include fever, chills, and constitutional symptoms of fatigue, malaise, anxiety, or confusion. These symptoms are not pathognomonic for infection and may also be observed in a wide variety of noninfectious inflammatory conditions. In addition, they may be absent in patients with serious infections, especially in elderly individuals.
Because systemic inflammatory response syndrome (SIRS), sepsis, septic shock, and multiple organ dysfunction syndrome (MODS) represent a clinical continuum (see Overview), the specific features exhibited in any given case depend on where the patient falls on that continuum.
Fever is a common feature of sepsis. Fever of infectious origin results from resetting the hypothalamus so that heat production and heat loss are balanced to maintain a higher temperature. An abrupt onset of fever usually is associated with a large infectious load.
Chills are a secondary symptom associated with fever and result from increased muscular activity in an attempt to produce heat and thereby raise the body temperature to the level required to reset the hypothalamus.
Sweating occurs when the hypothalamus returns to its normal set point and senses that the body temperature is above the desired level. Perspiration is stimulated to offload excess body heat through evaporative cooling.
Altered mental function is often observed. Mild disorientation or confusion is especially common in elderly individuals. More severe manifestations include apprehension, anxiety, and agitation, and in some cases, coma may eventually ensue. The mechanism by which mental function is altered is not known, but altered amino acid metabolism has been proposed as a cause of metabolic encephalopathy.
Hyperventilation with respiratory alkalosis is a common feature of sepsis. Stimulation of the medullary ventilatory center by endotoxins and other inflammatory mediators has been proposed as the cause of hyperventilation.
The following localizing symptoms are some of the most useful clues to the etiology of both fever and sepsis:
Head and neck infections - Earache, sore throat, sinus pain, or swollen lymph glands
Chest and pulmonary infections - Cough (especially if productive), pleuritic chest pain, and dyspnea
Abdominal and gastrointestinal (GI) infections - Abdominal pain, nausea, vomiting, and diarrhea
Pelvic and genitourinary (GU) infections - Pelvic or flank pain, vaginal or urethral discharge, urea, frequency, urgency
Bone and soft tissue infections - Focal pain or tenderness, focal erythema, edema
The physical examination focuses first on the general condition of the patient. Assess the patient’s overall hemodynamic condition to search for signs of hyperperfusion. Look for signs suggestive of a focal infection. An acutely ill, toxic appearance is a common feature in patients with serious infections.
The vital signs may suggest sepsis, even if fever is absent. As noted (see above), tachypnea is common; tachycardia with an increased pulse pressure also is common.
Measure the body temperature accurately. Because oral temperatures are often unreliable, rectal temperatures should be obtained.
Investigate signs of systemic tissue perfusion. In the early stages of sepsis, cardiac output is well maintained or even increased. Along with the effects of vasodilatory mediators, this may result in warm skin, warm extremities, and normal capillary refill. As sepsis progresses, stroke volume and cardiac output fall. Patients begin to manifest signs of poor distal perfusion, including cool skin, cool extremities, and delayed capillary refill.
The following physical signs suggest focal, usually bacterial, infection:
Central nervous system (CNS) infection - Profound depression in mental status and meningismus
Head and neck infections - Inflamed or swollen tympanic membranes, sinus tenderness, pharyngeal exudates, stridor, cervical lymphadenopathy
Chest and pulmonary infections - Localized rales or evidence of consolidation
Cardiac infections - Regurgitant valvular murmur
Abdominal and GI infections - Focal tenderness, guarding or rebound, rectal tenderness, or swelling
Pelvic and GU infections - Costovertebral angle tenderness, pelvic tenderness, cervical motion pain, and adnexal tenderness
Bone and soft tissue infections - Focal erythema, edema, infusion, and tenderness
Skin infections - Petechiae and purpura
Baue AE. Multiple, progressive, or sequential systems failure. A syndrome of the 1970s. Arch Surg. 1975 Jul. 110(7):779-81. [Medline].
Gustot T. Multiple organ failure in sepsis: prognosis and role of systemic inflammatory response. Curr Opin Crit Care. 2011 Apr. 17(2):153-9. [Medline].
Bone RC, Balk RA, Cerra FB, 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. 1992. Chest. 2009 Nov. 136(5 Suppl):e28. [Medline].
Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23. 315 (8):801-10. [Medline].
Vincent JL, Moreno R, Takala J, Willatts S, De Mendonça A, Bruining H, et al. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. Intensive Care Med. 1996 Jul. 22 (7):707-10. [Medline].
Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, et al. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23. 315 (8):762-74. [Medline].
Harrois A, Huet O, Duranteau J. Alterations of mitochondrial function in sepsis and critical illness. Curr Opin Anaesthesiol. 2009 Apr. 22(2):143-9. [Medline].
Uchino S, Kellum JA, Bellomo R, Doig GS, Morimatsu H, Morgera S. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005 Aug 17. 294(7):813-8. [Medline].
Ruf W. New players in the sepsis-protective activated protein C pathway. J Clin Invest. 2010 Sep. 120(9):3084-7. [Medline].
Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013 Aug 29. 369(9):840-51. [Medline].
Adrie C, Alberti C, Chaix-Couturier C, Azoulay E, De Lassence A, Cohen Y. Epidemiology and economic evaluation of severe sepsis in France: age, severity, infection site, and place of acquisition (community, hospital, or intensive care unit) as determinants of workload and cost. J Crit Care. 2005 Mar. 20(1):46-58. [Medline].
Brun-Buisson C, Doyon F, Carlet J. Bacteremia and severe sepsis in adults: a multicenter prospective survey in ICUs and wards of 24 hospitals. French Bacteremia-Sepsis Study Group. Am J Respir Crit Care Med. 1996 Sep. 154(3 Pt 1):617-24. [Medline].
Martin CM, Priestap F, Fisher H, et al. A prospective, observational registry of patients with severe sepsis: the Canadian Sepsis Treatment and Response Registry. Crit Care Med. 2009 Jan. 37(1):81-8. [Medline].
Brun-Buisson C. The epidemiology of the systemic inflammatory response. Intensive Care Med. 2000. 26 Suppl 1:S64-74. [Medline].
Brun-Buisson C, Doyon F, Carlet J, Dellamonica P, Gouin F, Lepoutre A, et al. Incidence, risk factors, and outcome of severe sepsis and septic shock in adults. A multicenter prospective study in intensive care units. French ICU Group for Severe Sepsis. JAMA. 1995 Sep 27. 274(12):968-74. [Medline].
Lobo SM, Rezende E, Knibel MF, et al. Early determinants of death due to multiple organ failure after noncardiac surgery in high-risk patients. Anesth Analg. 2011 Apr. 112(4):877-83. [Medline].
Shapiro NI, Trzeciak S, Hollander JE, et al. A prospective, multicenter derivation of a biomarker panel to assess risk of organ dysfunction, shock, and death in emergency department patients with suspected sepsis. Crit Care Med. 2009 Jan. 37(1):96-104. [Medline].
Nelson DP, Lemaster TH, Plost GN, Zahner ML. Recognizing sepsis in the adult patient. Am J Nurs. 2009 Mar. 109(3):40-5; quiz 46. [Medline].
Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013 Feb. 41(2):580-637. [Medline].
De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010 Mar 4. 362(9):779-89. [Medline].
Patel GP, Grahe JS, Sperry M, et al. Efficacy and safety of dopamine versus norepinephrine in the management of septic shock. Shock. 2010 Apr. 33(4):375-80. [Medline].
Bernard GR, Vincent JL, Laterre PF, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med. 2001 Mar 8. 344(10):699-709. [Medline].
Angus DC. Drotrecogin alfa (activated) ... a sad final fizzle to a roller-coaster party. Crit Care. 2012 Feb 6. 16(1):107. [Medline].
Briegel J, Forst H, Haller M, et al. Stress doses of hydrocortisone reverse hyperdynamic septic shock: a prospective, randomized, double-blind, single-center study. Crit Care Med. 1999 Apr. 27(4):723-32. [Medline].
Nathens AB, Marshall JC. Selective decontamination of the digestive tract in surgical patients: a systematic review of the evidence. Arch Surg. 1999 Feb. 134(2):170-6. [Medline].
|Organ System||Mild Criteria||Severe Criteria|
|Pulmonary||Hypoxia or hypercarbia necessitating assisted ventilation for 3-5 days||ARDS requiring PEEP >10 cm H2 O and FI O2 < 0.5|
|Hepatic||Bilirubin 2-3 mg/dL or other liver function tests >2 × normal, PT elevated to 2 × normal||Jaundice with bilirubin 8-10 mg/dL|
|Renal||Oliguria (< 500 mL/day) or increasing creatinine (2-3 mg/dL)||Dialysis|
|Gastrointestinal||Intolerance of gastric feeding for more than 5 days||Stress ulceration with need for transfusion, acalculous cholecystitis|
|Hematologic||aPTT >125% of normal, platelets < 50-80,000||DIC|
|Cardiovascular||Decreased ejection fraction with persistent capillary leak||Hyperdynamic state not responsive to pressors|
|Peripheral nervous system||Mild sensory neuropathy||Combined motor and sensory deficit|
|aPTT = activated partial thromboplastin time; ARDS = acute respiratory distress syndrome; CNS = central nervous system; DIC = disseminated intravascular coagulation; FI O2 = fraction of inspired oxygen; PEEP = positive end-expiratory pressure; PT = prothrombin time.|