Multiple Organ Dysfunction Syndrome in Sepsis Clinical Presentation

  • Author: Ali H Al-Khafaji, MD, MPH; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM   more...
 
Updated: Apr 12, 2012
 

History

Symptoms of sepsis are usually nonspecific and include fever, chills, and constitutional symptoms of fatigue, malaise, anxiety, or confusion.[12] 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
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Physical Examination

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
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Contributor Information and Disclosures
Author

Ali H Al-Khafaji, MD, MPH  Associate Professor of Critical Care Medicine, Director, Transplant Intensive Care Unit, University of Pittsburgh School of Medicine

Ali H Al-Khafaji, MD, MPH is a member of the following medical societies: American College of Chest Physicians, American College of Gastroenterology, American College of Physicians, and International Liver Transplantation Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC  Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Gregg Eschun, MD  Assistant Professor, Department of Internal Medicine, Sections of Respirology and Critical Care, St Boniface Hospital, University of Manitoba Faculty of Medicine, Canada

Gregg Eschun, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Canadian Medical Association, and College of Physicians and Surgeons of Manitoba

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 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; Applied Physiology, Ltd Honoraria Consulting; Cheetah Medical Consulting fee 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.

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. Baue AE. Multiple, progressive, or sequential systems failure. A syndrome of the 1970s. Arch Surg. Jul 1975;110(7):779-81. [Medline].

  2. Gustot T. Multiple organ failure in sepsis: prognosis and role of systemic inflammatory response. Curr Opin Crit Care. Apr 2011;17(2):153-9. [Medline].

  3. 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. Nov 2009;136(5 Suppl):e28. [Medline].

  4. Harrois A, Huet O, Duranteau J. Alterations of mitochondrial function in sepsis and critical illness. Curr Opin Anaesthesiol. Apr 2009;22(2):143-9. [Medline].

  5. 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. Mar 2005;20(1):46-58. [Medline].

  6. 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. Sep 1996;154(3 Pt 1):617-24. [Medline].

  7. 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. Jan 2009;37(1):81-8. [Medline].

  8. Blanco J, Muriel-Bombín A, Sagredo V, et al. Incidence, organ dysfunction and mortality in severe sepsis: a Spanish multicentre study. Crit Care. 2008;12(6):R158. [Medline].

  9. Brun-Buisson C. The epidemiology of the systemic inflammatory response. Intensive Care Med. 2000;26 Suppl 1:S64-74. [Medline].

  10. 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. Sep 27 1995;274(12):968-74. [Medline].

  11. 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. Apr 2011;112(4):877-83. [Medline].

  12. 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. Jan 2009;37(1):96-104. [Medline].

  13. Nelson DP, Lemaster TH, Plost GN, Zahner ML. Recognizing sepsis in the adult patient. Am J Nurs. Mar 2009;109(3):40-5; quiz 46. [Medline].

  14. Jaimes F, De La Rosa G, Morales C, et al. Unfractioned heparin for treatment of sepsis: A randomized clinical trial (The HETRASE Study). Crit Care Med. Apr 2009;37(4):1185-96. [Medline].

  15. De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. Mar 4 2010;362(9):779-89. [Medline].

  16. Patel GP, Grahe JS, Sperry M, et al. Efficacy and safety of dopamine versus norepinephrine in the management of septic shock. Shock. Apr 2010;33(4):375-80. [Medline].

  17. Bernard GR, Vincent JL, Laterre PF, 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].

  18. Angus DC. Drotrecogin alfa (activated) ... a sad final fizzle to a roller-coaster party. Crit Care. Feb 6 2012;16(1):107. [Medline].

  19. 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. Apr 1999;27(4):723-32. [Medline].

  20. van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, et al. Intensive insulin therapy in critically ill patients. N Engl J Med. Nov 8 2001;345(19):1359-67. [Medline].

  21. 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].

  22. Nathens AB, Marshall JC. Selective decontamination of the digestive tract in surgical patients: a systematic review of the evidence. Arch Surg. Feb 1999;134(2):170-6. [Medline].

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Stages of sepsis based on American College of Chest Physicians/Society of Critical Care Medicine Consensus Panel guidelines.
Pathogenesis of sepsis and multiorgan failure.
Venn diagram showing overlap of infection, bacteremia, sepsis, systemic inflammatory response syndrome (SIRS), and multiorgan dysfunction.
Acute respiratory distress syndrome (ARDS) present in this chest x-ray (CXR) film is a common organ system affected in multiorgan failure of sepsis.
Acute respiratory distress syndrome (ARDS) shown in this chest x-ray (CXR) film is a common complication of septic shock. Note bilateral airspace infiltration, absence of cardiomegaly, vascular redistribution, and Kerley B lines.
Organizing phase of diffuse alveolar damage (ARDS) secondary to septic shock shows diffuse alveolar injury and infiltration with inflammatory cells.
Organizing diffuse alveolar damage in a different location showing disorganization of pulmonary architecture.
A high-power view of organizing diffuse alveolar damage (ARDS) shows hyperplasia of type II pneumocytes and hyaline membrane deposits.
Table. Criteria for Organ Dysfunction
Organ System Mild Criteria Severe Criteria
PulmonaryHypoxia or hypercarbia necessitating assisted ventilation for 3-5 daysARDS requiring PEEP >10 cm H2 O and FI O2 < 0.5
HepaticBilirubin 2-3 mg/dL or other liver function tests >2 × normal, PT elevated to 2 × normalJaundice with bilirubin 8-10 mg/dL
RenalOliguria (< 500 mL/day) or increasing creatinine (2-3 mg/dL)Dialysis
GastrointestinalIntolerance of gastric feeding for more than 5 daysStress ulceration with need for transfusion, acalculous cholecystitis
HematologicaPTT >125% of normal, platelets < 50-80,000DIC
CardiovascularDecreased ejection fraction with persistent capillary leakHyperdynamic state not responsive to pressors
CNSConfusionComa
Peripheral nervous systemMild sensory neuropathyCombined 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.
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