Systemic inflammatory response syndrome

Last updated
Systemic inflammatory response syndrome
Specialty Immunology
Complications Acute kidney injury, shock, septic shock, sepsis, multiple organ failure

In immunology, systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body. [1] It is the body's response to an infectious or noninfectious insult. Although the definition of SIRS refers to it as an "inflammatory" response, it actually has pro- and anti-inflammatory components.

Contents

Presentation

Complications

SIRS is frequently complicated by failure of one or more organs or organ systems. [2] [3] [4] The complications of SIRS include

Causes

The causes of SIRS are broadly classified as infectious or noninfectious. Causes of SIRS include:[ citation needed ]

Other causes include: [2] [3] [4]

Diagnosis

Systemic inflammatory response syndrome [5]
FindingValue
Temperature <36 °C (96.8 °F) or >38 °C (100.4 °F)
Heart rate >90/min
Respiratory rate >20/min or PaCO2<32 mmHg (4.3 kPa)
WBC <4x109/L (<4000/mm3), >12x109/L (>12,000/mm3), or ≥10% bands

SIRS is a serious condition related to systemic inflammation, organ dysfunction, and organ failure. It is a subset of cytokine storm, in which there is abnormal regulation of various cytokines. [6] SIRS is also closely related to sepsis, in which patients satisfy criteria for SIRS and have a suspected or proven infection. [2] [3] [4] [7]

Many experts consider the current criteria for a SIRS diagnosis to be overly sensitive, as nearly all (>90%) of patients admitted to the ICU meet the SIRS criteria. [8]

Adult

Manifestations of SIRS include, but are not limited to: [9]

When two or more of these criteria are met with or without evidence of infection, patients may be diagnosed with "SIRS". Patients with SIRS and acute organ dysfunction may be termed "severe SIRS". [3] [4] [10] Note: Fever and an increased white blood cell count are features of the acute-phase reaction, while an increased heart rate is often the initial sign of hemodynamic compromise. An increased rate of breathing may be related to the increased metabolic stress due to infection and inflammation, but may also be an ominous sign of inadequate perfusion resulting in the onset of anaerobic cellular metabolism.[ citation needed ]

Children

The International Pediatric Sepsis Consensus has proposed some changes to adapt these criteria to the pediatric population. [11]

In children, the SIRS criteria are modified in the following fashion: [11]

Temperature or white blood cell count must be abnormal to qualify as SIRS in pediatric patients. [11]

Treatment

Generally, the treatment for SIRS is directed towards the underlying problem or inciting cause (i.e. adequate fluid replacement for hypovolemia, IVF/NPO for pancreatitis, epinephrine/steroids/diphenhydramine for anaphylaxis). [12] Selenium, glutamine, and eicosapentaenoic acid have shown effectiveness in improving symptoms in clinical trials. [13] [14] Other antioxidants such as vitamin E may be helpful as well. [15]

Septic treatment protocol and diagnostic tools have been created due to the potentially severe outcome septic shock. For example, the SIRS criteria were created as mentioned above to be extremely sensitive in suggesting which patients may have sepsis. However, these rules lack specificity, i.e. not a true diagnosis of the condition, but rather a suggestion to take necessary precautions. The SIRS criteria are guidelines set in place to ensure septic patients receive care as early as possible. [5]

In cases caused by an implanted mesh, removal (explantation) of the polypropylene surgical mesh implant may be indicated. [16]

History

The concept of SIRS was first conceived of and presented by William R. Nelson, of the Department of Surgery of the University of Toronto. SIRS was more broadly adopted in 1991 at the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference with the goal of aiding in the early detection of sepsis. [17]

Criteria for SIRS were established in 1992 as part of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. [2] The conference concluded that the manifestations of SIRS include, but are not limited to the first four described above under adult SIRS criteria.[ citation needed ]

In septic patients, these clinical signs can also be seen in other proinflammatory conditions, such as trauma, burns, pancreatitis, etc. A follow-up conference, therefore, decided to define the patients with a documented or highly suspicious infection that results in a systemic inflammatory response as having sepsis. [18] Note that SIRS criteria are non-specific, [18] and must be interpreted carefully within the clinical context. These criteria exist primarily for the purpose of more objectively classifying critically ill patients so that future clinical studies may be more rigorous and more easily reproducible.[ citation needed ]

Related Research Articles

<span class="mw-page-title-main">Lemierre's syndrome</span> Medical condition

Lemierre's syndrome is infectious thrombophlebitis of the internal jugular vein. It most often develops as a complication of a bacterial sore throat infection in young, otherwise healthy adults. The thrombophlebitis is a serious condition and may lead to further systemic complications such as bacteria in the blood or septic emboli.

<span class="mw-page-title-main">Shock (circulatory)</span> Medical condition of insufficient blood flow

Shock is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system. Initial symptoms of shock may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest, as complications worsen.

<span class="mw-page-title-main">Sepsis</span> Life-threatening organ dysfunction triggered by infection

Sepsis is a potentially life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs.

<span class="mw-page-title-main">Pleural effusion</span> Accumulation of excess fluid in the pleural cavity

A pleural effusion is accumulation of excessive fluid in the pleural space, the potential space that surrounds each lung. Under normal conditions, pleural fluid is secreted by the parietal pleural capillaries at a rate of 0.6 millilitre per kilogram weight per hour, and is cleared by lymphatic absorption leaving behind only 5–15 millilitres of fluid, which helps to maintain a functional vacuum between the parietal and visceral pleurae. Excess fluid within the pleural space can impair inspiration by upsetting the functional vacuum and hydrostatically increasing the resistance against lung expansion, resulting in a fully or partially collapsed lung.

<span class="mw-page-title-main">Septic shock</span> Dangerously low blood pressure due to damage from an organ infection

Septic shock is a potentially fatal medical condition that occurs when sepsis, which is organ injury or damage in response to infection, leads to dangerously low blood pressure and abnormalities in cellular metabolism. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) defines septic shock as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by requiring a vasopressor to maintain a mean arterial pressure of 65 mm Hg or greater and having serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%.

<span class="mw-page-title-main">Acute respiratory distress syndrome</span> Human disease

Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). For those who survive, a decreased quality of life is common.

In immunology, cytokine release syndrome (CRS) is a form of systemic inflammatory response syndrome (SIRS) that can be triggered by a variety of factors such as infections and certain drugs. It refers to cytokine storm syndromes (CSS) and occurs when large numbers of white blood cells are activated and release inflammatory cytokines, which in turn activate yet more white blood cells. CRS is also an adverse effect of some monoclonal antibody medications, as well as adoptive T-cell therapies. When occurring as a result of a medication, it is also known as an infusion reaction.

<span class="mw-page-title-main">Procalcitonin</span> Precursor of the peptide hormone calcitonin

Procalcitonin (PCT) is a peptide precursor of the hormone calcitonin, the latter being involved with calcium homeostasis. It arises once preprocalcitonin is cleaved by endopeptidase. It was first identified by Leonard J. Deftos and Bernard A. Roos in the 1970s. It is composed of 116 amino acids and is produced by parafollicular cells of the thyroid and by the neuroendocrine cells of the lung and the intestine.

Multiple organ dysfunction syndrome (MODS) is altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis.

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<span class="mw-page-title-main">SOFA score</span> Medical assessment

The sequential organ failure assessment score, previously known as the sepsis-related organ failure assessment score, is used to track a person's status during the stay in an intensive care unit (ICU) to determine the extent of a person's organ function or rate of failure. The score is based on six different scores, one each for the respiratory, cardiovascular, hepatic, coagulation, renal and neurological systems.

Catastrophic antiphospholipid syndrome (CAPS), also known as Asherson's syndrome, is a rare autoimmune disease in which widespread, intravascular clotting causes multi-organ failure. The syndrome is caused by antiphospholipid antibodies that target a group of proteins in the body that are associated with phospholipids. These antibodies activate endothelial cells, platelets, and immune cells, ultimately causing a large inflammatory immune response and widespread clotting. CAPS was first described by Ronald Asherson in 1992. The syndrome exhibits thrombotic microangiopathy, multiple organ thromboses, and in some cases tissue necrosis and is considered an extreme or catastrophic variant of the antiphospholipid syndrome.

End organ damage is severe impairment of major body organs due to high blood pressure or states of low blood pressure or low blood volume. This can present as a heart attack or heart failure, pulmonary edema, neurologic deficits including a stroke, or acute kidney failure.

<span class="mw-page-title-main">Hemophagocytic lymphohistiocytosis</span> Immune disorder in the blood leading to hyperinflammation

In hematology, hemophagocytic lymphohistiocytosis (HLH), also known as haemophagocytic lymphohistiocytosis, and hemophagocytic or haemophagocytic syndrome, is an uncommon hematologic disorder seen more often in children than in adults. It is a life-threatening disease of severe hyperinflammation caused by uncontrolled proliferation of benign lymphocytes and macrophages that secrete high amounts of inflammatory cytokines. It is classified as one of the cytokine storm syndromes. There are inherited and non-inherited (acquired) causes of HLH.

Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are overlapping syndromes of diffuse, symmetric, flaccid muscle weakness occurring in critically ill patients and involving all extremities and the diaphragm with relative sparing of the cranial nerves. CIP and CIM have similar symptoms and presentations and are often distinguished largely on the basis of specialized electrophysiologic testing or muscle and nerve biopsy. The causes of CIP and CIM are unknown, though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome. Corticosteroids and neuromuscular blocking agents, which are widely used in intensive care, may contribute to the development of CIP and CIM, as may elevations in blood sugar, which frequently occur in critically ill patients.

Critical illness–related corticosteroid insufficiency is a form of adrenal insufficiency in critically ill patients who have blood corticosteroid levels which are inadequate for the severe stress response they experience. Combined with decreased glucocorticoid receptor sensitivity and tissue response to corticosteroids, this adrenal insufficiency constitutes a negative prognostic factor for intensive care patients.

Renal angina is a clinical methodology to risk stratify patients for the development of persistent and severe acute kidney injury (AKI). The composite of risk factors and early signs of injury for AKI, renal angina is used as a clinical adjunct to help optimize the use of novel AKI biomarker testing. The term angina from Latin and from the Greek ankhone ("strangling") are utilized in the context of AKI to denote the development of injury and the choking off of kidney function. Unlike angina pectoris, commonly caused due to ischemia of the heart muscle secondary to coronary artery occlusion or vasospasm, renal angina carries no obvious physical symptomatology. Renal angina was derived as a conceptual framework to identify evolving AKI. Like acute coronary syndrome which precedes or is a sign of a heart attack, renal angina is used as a herald sign for a kidney attack. Detection of renal angina is performed by calculating the renal angina index.

Acute eosinophilic pneumonia (AEP) is an uncommon, acute-onset form of eosinophilic lung disease which varies in severity. Though poorly understood, the pathogenesis of AEP likely varies depending on the underlying cause which may include smoking, inhalation exposure, medication, and infection.[3] In most patients, AEP is idiopathic, or has no known cause.[1]

Vasodilatory shock, vasogenic shock, or vasoplegic shock is a medical emergency belonging to shock along with cardiogenic shock, septic shock, allergen-induced shock and hypovolemic shock. When the blood vessels suddenly relax, it results in vasodilation. In vasodilatory shock, the blood vessels are too relaxed leading to extreme vasodilation and blood pressure drops and blood flow becomes very low. Without enough blood pressure, blood and oxygen will not be pushed to reach the body's organs. If vasodilatory shock lasts more than a few minutes, the lack of oxygen starts to damage the body's organs. Vasodilatory shock like other types of shock should be treated quickly, otherwise it can cause permanent organ damage or death as a result of multiple organ dysfunction.

<span class="mw-page-title-main">Multisystem inflammatory syndrome in children</span> Disease of children; pediatric comorbidity from COVID-19

Multisystem inflammatory syndrome in children (MIS-C), or paediatric inflammatory multisystem syndrome, or systemic inflammatory syndrome in COVID-19 (SISCoV), is a rare systemic illness involving persistent fever and extreme inflammation following exposure to SARS-CoV-2, the virus responsible for COVID-19. MIS-C has also been monitored as a potential, rare pediatric adverse event following COVID-19 vaccination. It can rapidly lead to medical emergencies such as insufficient blood flow around the body. Failure of one or more organs can occur. A warning sign is unexplained persistent fever with severe symptoms following exposure to COVID-19. Prompt referral to paediatric specialists is essential, and families need to seek urgent medical assistance. Most affected children will need intensive care.

References

  1. ↑ Jaffer U, Wade RG, Gourlay T (2010). "Cytokines in the systemic inflammatory response syndrome: a review". HSR Proc Intensive Care Cardiovasc Anesth. 2 (3): 161–75. ISSN   2037-0504. PMC   3484588 . PMID   23441054.
  2. 1 2 3 4 "American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis" (PDF). Crit. Care Med. 20 (6): 864–74. 1992. doi:10.1097/00003246-199206000-00025. PMID   1597042. S2CID   20057097. Archived from the original (PDF) on 2013-10-17.
  3. 1 2 3 4 Rippe JM, Irwin RS, Cerra FB (1999). Irwin and Rippe's intensive care medicine. Philadelphia: Lippincott-Raven. ISBN   0-7817-1425-7.
  4. 1 2 3 4 Marino PL (1998). The ICU book. Baltimore: Williams & Wilkins. ISBN   0-683-05565-8.
  5. 1 2 Bone RC, Balk RA, et al. (The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine) (June 1992). "Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis". Chest . 101 (6): 1644–55. doi:10.1378/chest.101.6.1644. PMID   1303622.
  6. ↑ Parsons M (2010). "Cytokine storm in the pediatric oncology patient" (PDF). J Pediatr Oncol Nurs. 27 (5): 253–8. doi:10.1177/1043454210368533. PMID   20736486. S2CID   206624494. Archived from the original (PDF) on 2016-03-03. Retrieved 2011-04-04.
  7. ↑ Kalil A (2020-10-07). "Septic Shock". Medscape.updated
  8. ↑ Lord JM, Midwinter MJ, Chen YF, Belli A, Brohi K, Kovacs EJ, Koenderman L, Kubes P, Lilford RJ (October 2014). "The systemic immune response to trauma: an overview of pathophysiology and treatment". Lancet. 384 (9952): 1455–65. doi:10.1016/S0140-6736(14)60687-5. PMC   4729362 . PMID   25390327.
  9. ↑ Comstedt P, Storgaard M, Lassen AT (December 2009). "The Systemic Inflammatory Response Syndrome (SIRS) in acutely hospitalised medical patients: a cohort study". Scand J Trauma Resusc Emerg Med. 17: 67. doi: 10.1186/1757-7241-17-67 . PMC   2806258 . PMID   20035633.
  10. ↑ Tsiotou AG, Sakorafas GH, Anagnostopoulos G, Bramis J (March 2005). "Septic shock; current pathogenetic concepts from a clinical perspective". Med Sci Monit. 11 (3): RA76–85. PMID   15735579.
  11. 1 2 3 Goldstein B, Giroir B, Randolph A (January 2005). "International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics". Pediatr Crit Care Med. 6 (1): 2–8. doi:10.1097/01.PCC.0000149131.72248.E6. ISSN   1529-7535. PMID   15636651. S2CID   8190072.
  12. ↑ Boka K (2019-06-26). "Systemic Inflammatory Response Syndrome Treatment & Management". Medscape.
  13. ↑ Berger MM, Chioléro RL (September 2007). "Antioxidant supplementation in sepsis and systemic inflammatory response syndrome". Crit Care Med. 35 (9 Suppl): S584–90. doi:10.1097/01.CCM.0000279189.81529.C4. PMID   17713413. S2CID   21329654.
  14. ↑ Rinaldi S, Landucci F, De Gaudio AR (September 2009). "Antioxidant therapy in critically septic patients". Curr Drug Targets. 10 (9): 872–80. doi:10.2174/138945009789108774. PMID   19799541.
  15. ↑ Bulger EM, Maier RV (February 2003). "An argument for Vitamin E supplementation in the management of systemic inflammatory response syndrome". Shock. 19 (2): 99–103. doi: 10.1097/00024382-200302000-00001 . PMID   12578114. S2CID   35863434.
  16. ↑ Voyles CR, Richardson JD, Bland KI, Tobin GR, Flint LM, Polk HC (August 1981). "Emergency abdominal wall reconstruction with polypropylene mesh: short-term benefits versus long-term complications". Ann Surg. 194 (2): 219–23. doi:10.1097/00000658-198108000-00017. PMC   1345243 . PMID   6455099.
  17. ↑ "CHEST Home".
  18. 1 2 Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, Cohen J, Opal SM, Vincent JL, Ramsay G (April 2003). "2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference". Crit Care Med. 31 (4): 1250–6. doi:10.1097/01.CCM.0000050454.01978.3B. PMID   12682500. S2CID   19605781.
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