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Definitions of systemic inflammatory response syndrome (SIRS), sepsis, septic shock, and multiple organ dysfunction syndrome

Systemic inflammatory response syndrome

Two or more of the following clinical signs of systemic response to endothelial inflammation:


• Temperature > 38°C or < 36°C
x Heart rate > 90 beats/min

• Tachypnoea (respiratory rate > 20 breaths/min or hyperventilation (Paco2 < 4.25 kPa))

• White blood cell count > 12 ⋅ 109/l or < 4 ⋅ 109/l or the presence of more than 10% immature neutrophils
In the setting (or strong suspicion) of a known cause of endothelial inflammation such as:

• Infection (bacteria, viruses, fungi, parasites, yeasts, or other organisms)

• Pancreatitis
x Ischaemia
x Multiple trauma and tissue injury
x Haemorrhagic shock
x Immune mediated organ injury
x Absence of any other known cause for such clinical abnormalities

Sepsis

Systemic response to infection manifested by two or more of the following:


• Temperature > 38°C or < 36°C
x Raised heart rate > 90/min

• Tachypnoea (respiratory rate > 20 breaths/min or hyperventilation (Paco2 < 4.25 kPa))

• White blood cell count > 12 × 109/l or < 4 × 109/l or the presence of more than 10% immature neutrophils

Septic shock

Sepsis induced hypotension (systolic blood pressure < 90 mm Hg or a reduction of >40 mm Hg from baseline) despite adequate fluid resuscitation

Multiple organ dysfunction syndrome

Presence of altered organ function in an acutely ill patient such that homoeostasis cannot be maintained without intervention

Pathogenesis

Systemic sepsis may complicate an obvious primary infection such as community acquired pneumonia or a ruptured abdominal viscus. Frequently, however, an infective source cannot be identified and the type of organism cultured may provide no clue to its anatomical origin.

Infections that complicate critical illness may arise from the gastrointestinal tract. This region is particularly sensitive to poor perfusion, which may lead to increased bowel permeability and translocation of organisms and endotoxin from the lumen of the gastrointestinal tract into the portal venous and lymphatic circulations. The subsequent release of cytokines and other inflammatory mediators by hepatic Kupffer cells and circulating monocytes may then initiate a sequence of events that culminates in the clinical signs of sepsis and multiple organ failure.

Scientific background

The movement of oxygen, the regulation of its distribution between and within tissues, and the monitoring of cellular metabolism are all important in the clinical management of critically ill patients. Patients with sepsis or the systemic inflammatory response syndrome have a haemodynamic disturbance characterised by a raised cardiac output and reduced systemic vascular resistance. Although delivery of oxygen may be maintained or even increased by pharmacological means, most patients have poor peripheral uptake of oxygen.

The cause of this phenomenon remains unclear. However, sepsis and systemic inflammatory response syndrome are associated with damage to the vascular endothelium, which normally produces vasoactive substances that regulate microvascular blood flow to ensure that all organs are adequately oxygenated. The microcirculation may therefore be disrupted. In addition, inflammatory mediators may modulate directly the intracellular mechanisms that regulate use of oxygen, including mitochondrial function. These two factors mean that patients with sepsis or the systemic inflammatory response syndrome commonly develop multiple organ failure, to which many succumb. Nevertheless, not all patients at risk of developing sepsis and multiple organ failure do so, and individual susceptibility varies widely.

Each patient’s clinical response to the activation of inflammatory cascades may be determined by abnormalities of gene transcription and regulation that modulate the release of vasoactive substances such as nitric oxide, endothelins, and cyclo-oxygenase products (thromboxanes, prostaglandins, etc). Additionally, changes in the effectiveness of endogenous defence systems such as cellular antioxidant protection, repair, and apoptosis may be relevant in determining outcome. In any event, the clinical result of these perturbations is tissue hypoxia.

Detection of tissue hypoxia

The clinical signs of tissue hypoxia are largely non-specific. However, increased respiratory rate, peripheries that are either warm and vasodilated or cold and vasoconstricted, poor urine output, and mental dullness may indicate organ dysfunction and should prompt a search for reversible causes. The following biochemical and physiological measurements may be helpful.

Metabolic acidosis

A low arterial pH and high blood lactate concentration may be important. Anaerobic production of lactate may occur secondary to global hypoxia (for example, cardiorespiratory failure or septic shock) or focal hypoxia (for example, infarcted bowel) or through non-hypoxic causes (for example, delayed lactate clearance, accelerated aerobic glycolysis, or dysfunction of pyruvate dehydrogenase). A wide arterial-mixed venous carbon dioxide pressure gradient ( > 1 kPa) has been shown to be relatively insensitive as a marker of anaerobic tissue metabolism.

Oxygen extraction ratio

The uptake of oxygen by tissues (Vo2) is normally independent of oxygen delivery (Do2). If delivery fails the oxygen extraction ratio (Vo2:Do2) rises to maintain a constant rate of uptake and fulfil tissue demand. The compensatory mechanisms fail only at very low oxygen delivery levels (termed Do2Crit), when extraction starts to fall and become dependent on delivery. However, patients with sepsis or the systemic inflammatory response syndrome have a low oxygen extraction ratio, indicating poor tissue uptake or use. Changes in oxygen delivery and uptake relations have been used to identify occult tissue hypoxia and predict outcome since those who survive septic shock tend to achieve normal oxygen extraction levels.

Increasing oxygen delivery in these patients should produce a corresponding increase in uptake. However, in practice this is difficult to ascertain because of problems in measurement and the need for tissue oxygen demand to remain constant.

Recent randomised clinical trials have also indicated that patients receiving treatment designed to increase oxygen delivery and uptake may have greater mortality than controls. A high mixed venous oxygen saturation, measured through a pulmonary artery catheter, indirectly indicates a low oxygen extraction ratio.

Gastric mucosal pH (pHi)

Gastric mucosal pH can be measured using a tonometer, originally a saline filled balloon placed in the gastric lumen. If the arterial bicarbonate concentration is known, the carbon dioxide tension in the saline samples withdrawn from the balloon can be used to calculate the pH. Several studies have found that a falling or persistently low gastric mucosal pH is associated with poor prognosis in critically ill patients. However, whether gastric mucosal pH truly provides evidence of gastric mucosal hypoxia remains uncertain. Tonometers are now becoming semiautomated and use air instead of saline. Measurement of gastric-arterial carbon dioxide tension or gastric-end-tidal carbon dioxide tension differences has been suggested instead of gastric mucosal pH.

Injury to individual organs

Lung injury

About 35% of patients with sepsis develop mild to moderate acute lung injury and a quarter have fully developed acute respiratory distress syndrome. Affected patients have increased pulmonary vascular permeability, which leads to alveolar oedema and refractory hypoxaemia. Lung injury rarely occurs in isolation. It is usually the pulmonary manifestation of a pan-endothelial insult with inflammatory vascular dysfunction. The annual incidence of acute respiratory distress syndrome is about 6 cases per 100 000 population. Data on incidence and outcome of acute lung injury, which was defined relatively recently, are sparse.

Acute lung injury and the acute respiratory distress syndrome may have different causes as the acute respiratory distress syndrome is partly determined by the nature of the underlying or precipitating condition. Moreover, the precipitating condition and coexisting multiple organ failure dictate outcome. The increased permeability of the alveolar capillary membrane in these conditions suggests that lowering filling pressures by aggressive diuresis or early ultrafiltration may improve oxygenation. However, any concomitant decrease in cardiac output can result in an overall fall in oxygen delivery and may prejudice the perfusion of other organs.

Cardiovascular injury

Myocardial dysfunction also complicates sepsis and the systemic inflammatory response syndrome. Ventricular dilatation occurs in patients with septic shock, and the ejection fraction may be reduced to around 30% despite an overall rise in measured cardiac output. Patients who die tend to have had lower end diastolic volumes and less compliant ventricles during diastole than survivors. Normal volunteers given endotoxin also develop left ventricular dilatation during diastole, suggesting that cardiac function is greatly affected in septic shock. The cellular changes behind ventricular dilatation are unknown.

Systemic vascular resistance is also low in sepsis, possibly through overexpression of vasodilator substances such as nitric oxide and cyclo-oxygenase products in the vascular smooth muscle. The consequent loss of vasoregulation may result in poor distribution of perfusion and tissue hypoxia.

Optimisation of left ventricular filling pressure, inotropic support, and vasoconstrictors such as noradrenaline are all beneficial in septic shock. In addition, novel pressor agents such as nitric oxide synthase inhibitors have been advocated recently

for patients with refractory septic shock. Increased knowledge of the changes in vascular biology that characterise sepsis and the systemic inflammatory response syndrome may allow transient genetic manipulation of the expression of vasoactive mediators that control microvascular distribution of blood flow.

Renal failure

Acute renal failure is a common complication of sepsis and the systemic inflammatory response syndrome. This may reflect changes in the distribution of intrarenal blood flow between the cortex and medulla. The ability of patients to maintain intravascular homoeostasis may also be impaired. The early use of haemofiltration to correct fluid imbalance and (possibly) remove circulating inflammatory mediators has been advocated, but the benefits are unproved. It is essential to restore circulating volume and achieve an adequate blood pressure and cardiac output to prevent and treat acute renal failure.

Dysfunction of gastrointestinal tract

The bowel is particularly susceptible to ischaemic insults. Hypoperfusion of the gastrointestinal tract is thought to be important in the pathogenesis of multiple organ failure as outlined above. Hepatic dysfunction, possibly resulting from reduced blood flow relative to metabolic demand, is also common in critically ill patients. Maintaining adequate flow and perfusion pressure are the only proved treatments to correct these deficiencies. Inotropic drugs with dilator properties such as dopexamine may selectively enhance splanchnic perfusion and oxygenation. Nevertheless, well controlled trials of augmented oxygen transport (possibly guided by gastric tonometry) are needed to establish the role of the gastrointestinal tract in multiple organ failure.

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