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PubMed1998

Sweet's syndrome associated with systemic inflammatory response syndrome.

Septic shock is characterised by infection causing a systemic inflammatory response, end-organ failure and acute circulatory collapse. Treatment consists of antimicrobial therapy and the supportive management of multi-organ failure. We report a case of what we believed to be septic shock due to pyelonephritis in a patient whose condition continued to deteriorate despite conventional treatment until the diagnosis of Sweet's syndrome was made. Once she was started on high dose steroids, her condition improved and she made a full recovery. We believe this to be the first case of a severe systemic inflammatory response syndrome associated with Sweet's syndrome.

Anti-Inflammatory Agents↗
PubMed1994

Systemic inflammatory response syndrome: septic shock.

The systemic inflammatory response syndrome (SIRS) is the body's response to a multitude of chemical mediators. Conditions inciting the release of these mediators include bacterial sepsis, viremia, pancreatitis, trauma, neoplasia, heat stroke, and many others. The key to the successful management of SIRS lies in anticipation and not reaction. Resuscitation of the patient to supranormal levels, coupled with aggressive monitoring and support of target organs are essential.

Animals↗
PubMed1998

The systemic inflammatory response syndrome: definitions and aetiology.

Systemic inflammatory response syndrome (SIRS) is the clinical expression of the action of complex intrinsic mediators of the acute phase reaction. SIRS can be precipitated by events such as infection, trauma, pancreatitis, and surgery. At times, SIRS can compromise the function of various organ systems resulting in Multiple Organ Dysfunction Syndrome (MODS). SIRS and MODS are graded expressions of the inflammation associated with acute illness. Mild forms are frequent in general wards for both medical and surgical patients but those with severe forms require intensive care. Clinicians should learn to identify SIRS in their patients at an early stage to determine the underlying cause and treatment before the SIRS progresses to a more severe form.

Acute-Phase Reaction↗
PubMed1996

[Significance of systemic inflammatory response syndrome at cardiopulmonary bypass].

Systemic Inflammatory Response Syndrome (SIRS) is a new concept of entry criteria for sepsis. This concept, when applied to area of Multiple Organ Failure (MOF), is considered to be a preparatory state for MOF. To study the significance of SIRS state at cardiac surgery, we measured the body temperature, white blood cell count, respiratory rate and heart rate of 18 patients who underwent elective cardiac surgery, from the 1st post-operative day to the 7th post-operative day. We also measured Interleukin-6 and 8 (IL-6 and IL-8) to understand the relationship between the SIRS state and inflammatory cytokines just after cardiopulmonary bypass (CPB), at the 1st, 3rd and 6th postoperative day. The result was as follows: Patients with CPB more than 120 minutes have more frequency and longer duration of SIRS than patients with CPB less than 120 minutes. Serum levels of IL-8 at SIRS state were revealed statistically higher than at non-SIRS case. Duration of SIRS state was related to CPB time and serum levels of IL-6 and IL-8 just after CPB. We concluded that SIRS state is an indication for anti-cytokine therapy to prevent MOF, and it is important to shorten CPB time in order to decrease the duration of SIRS.

Cardiopulmonary Bypass↗
PubMed1999

Nitric oxide scavengers in the treatment of shock associated with systemic inflammatory response syndrome.

Shock associated with systemic inflammatory response syndrome (SIRS) is a form of distributive shock affecting over 200,000 patients per year in the US that results in 50% mortality. The role of NO in a variety of shock states has been extensively studied and has been shown to be the primary effector in endotoxin lipopolysaccharide (LPS)-induced hypotension attendant to shock associated with sepsis or presumed sepsis. NO has also been shown to be a myocardial depressant, an inhibitor of mitochondrial electron transport, an inducer of vascular leakage and an enhancer of LPS-induced cytokine release. Hence, it is involved in a wide variety of shock-related pathologies and is a key target for therapeutic intervention. Mechanism of action based therapies using NO scavengers represent a promising new approach. However, because NO is involved in such a wide variety of both physiological and pathophysiological processes, a therapy directed at NO must be selective in order to be both safe and effective. NO scavengers are comprised of two basic classes: organic molecules and metal complexes. Pyridoxalated haemoglobin polyoxyethylene conjugate (PHP) is a chemically-modified haemoglobin. It is the furthest advanced NO scavenger in clinical trials and is about to enter pivotal Phase 3 trials in patients with shock associated with SIRS.

Clinical Trials as Topic↗
PubMed1997

Interleukin 1 receptor antagonist gene expression in rat pituitary in the systemic inflammatory response syndrome: pathophysiological implications.

The systemic inflammatory response syndrome (SIRS) is characterized by endothelial cell activation causing a generalized inflammatory response and cytokine-mediated pathophysiological alterations. The pathophysiology of SIRS involves changes in the functioning of several endocrine glands, including the pituitary. SIRS-induced alterations in pituitary function include activation of the hypothalamic-pituitary adrenal (HPA) axis causing hypercortisolemia, the euthyroid sick syndrome, and cessation of reproductive function. These changes are in part mediated by cytokines, such as tumor necrosis factor alpha (TNF-alpha) and interleukin 1 (IL-1). IL-1 function depends on the local ratio of bioactive IL-1 and IL-1 receptor antagonist. Here we review our studies on IL-1 beta and IL-1ra mRNA levels in the pituitary in a rat model of SIRS. We have found that IL-1 beta mRNA peaked at 2 h after lipopolysaccharide (LPS) administration, increasing twelvefold over control values in the posterior pituitary and fivefold over controls in the anterior pituitary. IL-1ra mRNA levels peaked at 6 h post-LPS administration, later than those of IL-1 beta mRNA. IL-1ra mRNA levels increased tenfold in the anterior pituitary, but were induced only threefold in the posterior pituitary. IL-1ra gene expression is profoundly induced in the pituitary in vivo during systemic inflammation and its induction follows that of IL-1 beta, but it is differentially regulated and tissue-specific, occurring predominantly in the anterior pituitary. Future studies of the effects of IL-1 in the pituitary should take into account the local levels of IL-1ra.

Animals↗
PubMed1997

Multiple organ failure, multiple organ dysfunction syndrome, and systemic inflammatory response syndrome. Why no magic bullets?

The concept of multiple organ failure and related abnormalities was first developed in the 1970s. Multiple organ failure became evident when the support systems in intensive care units were able to keep patients alive long enough for multiple organ problems to develop in them. The high mortality of patients with multiple organ failure provided a focus for the problems that ultimately led to death for many patients in the intensive care unit. The frequency of infection, sepsis, or inflammation in producing multiple organ failure led to clinical trials of so-called magic bullets for the treatment of patients with sepsis. These trials have had either limited success or negative results, despite considerable evidence for efficacy or protection by such agents in experimental animals and in studies of normal human volunteers. I believe a major reason for these negative results has been the use of general entry criteria for the trials rather than the treatment of specific diseases or injuries.

Humans↗
PubMed1999

Extracellular phospholipases A2 in relation to systemic inflammatory response syndrome (SIRS) and systemic complications in severe acute pancreatitis.

The pathophysiology of severe acute pancreatitis (AP) resembles other conditions with systemic inflammatory response syndrome (SIRS) such as sepsis predisposing to remote organ failure. Because extracellular phospholipases A2 (PLA2) have been implicated in AP, their serum concentrations were analyzed with respect to SIRS and systemic complications in patients with severe AP. The serum samples were collected daily for 12 days in 57 patients with severe AP. SIRS, early organ complications, local complications, and outcome of AP were recorded. Time-resolved fluoroimmunoassays were used for group I and group II PLA2 measurements. Thirty-nine (68.4%) patients fulfilled the criteria of SIRS within 12 days from admission. Pancreatic necrosis was detected in 43 (75.4%) patients. Infected necrosis was found preoperatively or at operation in five (8.8%) patients. Twenty-six (45.6%) and eight (14.0%) patients had respiratory or renal failure, respectively. Seven (12.3%) patients died of their disease. All patients with systemic complications fulfilled the criteria of SIRS. The increasing number of positive SIRS criteria was associated with increased frequency of systemic complications. Pancreatic necrosis was not significantly associated with SIRS. The serum concentration of group II PLA2 was significantly higher in patients with SIRS (p < 0.05) compared with patients without from day 7 onward. The concentration of group II PLA2 increased (p < 0.01) in patients with SIRS but decreased in patients without. The serum concentration of group II PLA2 did not differ significantly with respect to systemic complications. The concentration of group I PLA2 decreased (p < 0.05) similarly in patients with and without SIRS or systemic complications during follow-up, respectively. Early systemic complications of severe AP are associated with SIRS with increasing frequency as the number of positive SIRS criteria increases. Group II PLA2 but not group I PLA2 may have pathophysiologic importance in severe AP-associated SIRS. Increasing serum concentration of group II PLA2 seems to reflect the ongoing systemic inflammation in severe AP-associated SIRS.

Acute Disease↗
PubMedDate not supplied

[Systemic inflammatory response syndrome in surgical patients with sepsis].

Systemic inflammatory response syndrome and sepsis are common in surgically treated patients. Systemic inflammatory response syndrome represents a major factor of morbidity and mortality in these patients. The pathogenesis of these syndromes has been increasingly clarified. The objective of this review is to present an overview of our current understanding of the physiology underlying these conditions.

Humans↗
PubMed2001

Systemic inflammatory response syndrome and acute neurological disease.

Systemic inflammatory response syndrome is a common clinical entity often presenting as a complication of neurological disease or trauma. Clear diagnostic criteria exist. Induced pathological mechanisms include both immunological and endothelial dysfunction, and coagulopathy, which may lead to multiple organ failure and significant morbidity. Possible therapeutic mechanisms are discussed, but this complex syndrome is poorly understood and successful treatment may depend on further research into control mechanisms.

Blood Coagulation Disorders↗
PubMedDate not supplied

A new method to detect systemic inflammatory response syndrome by continuous monitoring system: an experimental study in rats.

A continuous monitoring system was designed for detection of systemic inflammatory response syndrome (SIRS) using spectrum analyser and local temperature mapping system with deep body thermometer. This method demonstrated significant increases of heart and respiratory rates and deep body temperature from normal levels within 120 minutes after lipopolysaccharide administration in rats. Our monitoring system appears promising for clinical detection of SIRS in the early stages to prevent multiple organ failure.

Animals↗
PubMed2006

Rapid assay for plasma soluble E-selectin predicts the development of acute respiratory distress syndrome in patients with systemic inflammatory response syndrome.

A newly developed rapid immunoassay method for plasma soluble E-selectin (sES) was examined to determine whether it can predict the development of acute respiratory distress syndrome (ARDS) in critically ill patients with systemic inflammatory response syndrome (SIRS). Plasma levels of sES were measured on admission (day 1) to the emergency unit. Development of various types of organ failures including ARDS was compared in the first 5 days of admission (from day 1 to day 5) between patients with normal plasma levels of sES and those with elevated plasma levels of sES. Plasma levels of sES were determined using a newly developed latex agglutination method that takes 20 min to obtain the test results. The normal range of the plasma sES level was 4.8-29.7 ng/mL with this method. Among the patients examined, 22 patients showed elevated sES levels (D(A)E group) and 28 showed normal sES levels (D(A)N group). Development of ARDS was significantly higher in the D(A)E group (15/22, 68.2%) than in the D(A)N group (4/28, 14.3%) (P < 0.001) and that of cardiovascular system failure, renal failure, and coagulation system failure was also significantly higher in the D(A)E group than in the D(A)N group. The mortality rate at 28 days after admission was higher in the D(A)E group (27.3%) than in the D(A)N group (0%) (P < 0.05). Determination of sES levels by this new rapid assay method might be useful for prediction of the development of ARDS in critically ill patients with SIRS, a pathologic condition that has the potential risk for development of multiple organ failure.

Adolescent↗
PubMed1998

[The relationship between severe burn injury and systemic inflammatory response syndrome].

OBJECTIVE: To study course of systemic inflammatory response syndrome (SIRS). METHODS: The relationship was observed between SIRS and the effect of burn injury on cellular and humoral immunity between survivors. Nonsurvivors were also compared. The gastric mucosal pHi was measured. RESULTS: The SIRS initiated 22 hours after burn injury and peaked 3 days to 7 days postburn. Compared to the survivors significan increase of content of TNF and decrease of content of G-CSF were detected in the nonsurvivors serum. Obvious immunosuppression could be found. In patients with SIRS accompanied with infection or organ failure, marked increase of mortality was seen. The value of pHi was very low. CONCLUSION: Severe burn injury can lead to the release of massive inflammatory mediators. The second insult such as infection can further amplify the process leading to a vicious cycle of inflammation which cause tissue damage and immunosuppression. To prevent MODS, early diagnosis and treatment including organ supply, use of antibacterial agents, oxygen supply and immunity therapy were necesary.

Adolescent↗
PubMed2003

Somatosensory evoked potentials as predictor of systemic inflammatory response syndrome in pigs?

OBJECTIVE: Sepsis or systemic inflammatory response syndrome (SIRS) is often associated with encephalopathy (70%), which has been described as an early symptom resulting in several diseases. The present study investigated somatosensory evoked potentials (SEP) as an indicator or even a predictor of cerebral dysfunction evaluated in an experimental model of SIRS in pigs. METHODS: Eight Göttinger minipigs were included in the study. SIRS was mediated by induction of pancreatitis due to injection (ductus pancreaticus) of 500 mg/kg sodium taurocholate and 2.5 IU/kg enterokinase. Monitored parameters were: arterial blood-central venous-pulmonary arterial pressure, and cardiac output, systemic vascular resistance, and body temperature. SEP were recorded from centroparietal vs. frontal areas after electrical stimulation of the right forepaw. RESULTS: At least 33% loss of vascular resistance from baseline (SIRS criteria) occurred in all animals within 4-18 h. Baseline recordings in all anesthetized animals indicated primary cortical responses to electrical stimuli identified by peak latencies between 15-20 ms (SEP(P15-20)). Attenuations in the amplitudes with significant median decreases of 46% were observed at least 4 h before the defined hemodynamic SIRS criteria. CONCLUSIONS: The present data show a trend for the attenuation in SEP amplitudes as an indicator of systemic inflammatory response. SEP monitoring may be a sensitive marker of developing early changes in cerebral function due to SIRS-related encephalopathy.

Analysis of Variance↗
PubMed2002

Systemic inflammatory response syndrome associated with Sweet's syndrome.

PURPOSE: To describe the first pediatric report of systemic inflammatory response syndrome, shock, and multiple organ dysfunction syndrome associated with Sweet's syndrome. DESIGN: Case report. SETTING: Pediatric intensive care unit. PATIENTS: A patient with Sweet's syndrome and multiple organ dysfunction syndrome. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We report the case of a 7-yr-old female child with an acute nonlymphoblastic leukemia in complete remission after an autologous bone marrow transplantation, with a clinical picture of skin lesions and fever that met the criteria of Sweet's syndrome and developing systemic inflammatory response syndrome, septic shock, and multiple organ dysfunction syndrome. Her clinical condition worsened despite broad-spectrum antimicrobial therapy and standard measures of cardiovascular support. An infectious site could not be identified, and all culture results were negative. Her condition improved dramatically once steroid therapy was administered, and she made a full recovery. CONCLUSION: Although it is a rare condition, the diagnosis of Sweet's syndrome must be considered in a patient with the typical skin lesions and systemic inflammatory response syndrome. The correct diagnosis is of great clinical importance, because therapy with systemic steroids results in a fast and remarkable improvement.

Journal Article↗
PubMed2002

Oxidative stress in critically ill patients with systemic inflammatory response syndrome.

OBJECTIVE: To evaluate whether critically ill patients with systemic inflammatory response syndrome, on admission to an intensive care unit, had more severe oxidative stress than those without this syndrome. DESIGN: A prospective, cohort study. SETTING: A mixed medical and surgical adult intensive care unit with 12 beds. PATIENTS: A total of 68 consecutive patients admitted to the intensive care unit. INTERVENTIONS: Venous blood samples were routinely obtained within 24 hrs of admission. MEASUREMENTS AND MAIN RESULTS: Patients' plasma total antioxidant capacity, the lipid peroxidation products malondialdehyde and 4-hydroxynonenal, reduced sulfhydryl groups, and nitrites/nitrates were measured by spectrophotometric technique at admission to the intensive care unit. Myeloperoxidase (enzyme-linked immunosorbent assay) and polymorphonuclear elastase (immuno-activation assay) were also measured on admission to the intensive care unit. The patients with criteria of systemic inflammatory response syndrome (n = 20) had higher Acute Physiology and Chronic health Evaluation III scores (determined by collecting the worst value within 24 hrs after admission to the intensive care unit) and plasma concentrations of lipid peroxidation products and nitrites/nitrates and lower plasma concentration of reduced sulfhydryl groups and plasma total antioxidant capacity than patients without the syndrome (n = 48). Moreover, the markers for leukocyte activation, myeloperoxidase and polymorphonuclear elastase, presented higher concentrations in the plasma of patients with systemic inflammatory response syndrome. CONCLUSIONS: Patients admitted to the intensive care unit with criteria of systemic inflammatory response syndrome had a more severe oxidative stress than patients without this syndrome.

APACHE↗
PubMed2006

The expression of toll-like receptor 2, 4 of livers in mice with systemic inflammatory response syndrome.

BACKGROUND: The complicated pathogenesis of systemic inflammatory response syndrome (SIRS) is a hot topic in critical care medicine. In this study we explored the expression of toll-like receptor (TLR) 2, 4 of livers in SIRS mice and evaluated the role of TLR2, 4 in the pathogenesis of SIRS. METHODS: Forty BABL/C mice were randomly divided into 2 groups: control (n=20) and SIRS (n=20). SIRS model was induced by severe acute pancreatitis. Blood routine, blood amylase, glutamic pyruvic transaminase and temperature were measured. Histological changes of pancreases and livers were observed microscopically. The mRNA expressions of TLR2, 4 were detected by real-time polymerase chain reaction (PCR). The protein expressions of TLR2, 4 were examined by Western blot. RESULTS: Marked edema, inflammatory cell infiltration, hemorrhage, and necrosis were observed in the pancreases and livers of SIRS mice. The concentrations of amylase and glutamic pyruvic transaminase were increased significantly. Body temperature and white blood cell count were decreased. The mRNA and protein expressions of TLR2, 4 increased markedly in SIRS mice. Significant difference was observed between SIRS and control mice (P<0.01). CONCLUSION: The expressions of TLR2, 4 of livers were increased markedly in SIRS mice, indicating that TLR might play an important role in the pathogenesis of SIRS.

Animals↗