Clinical presentation and diagnosis
The clinical features of sepsis are varied and often relate to the precipitating infective or non-infective cause. In classic sepsis the patient will be warm, flushed and vasodilated with signs of the systemic inflammatory response syndrome. Presentation can, however, be insidious and non-specific, especially in the elderly or those with multiple co-morbidities. This group of patients may present with cool peripheries, low cardiac output and established organ failure.
The following clinical features may be present:
Patients with sepsis are usually warm, flushed and vasodilated. They are frequently hyperdynamic; tachycardic, hypotensive with a high cardiac output. Signs of reduced tissue perfusion, i.e. elevated serum lactate and low central venous oxygen saturation may be present. It is increasingly recognised that the rise in lactate seen in sepsis may reflect increased glycolysis and hypermetabolic state rather than pure tissue hypoxia. Prior to the availability of cardiac output monitoring, two phases of septic shock were described “warm shock” (as described above) and so-called “cold shock” characterised by signs of poor perfusion and low cardiac output. Patients with cold shock have inadequate cardiac output and typically require further fluid resuscitation and sometimes inotropic support.
Tachypnoea is often an early sign. As sepsis progresses pulmonary oedema and metabolic acidosis contribute to progressive hypoxaemia and respiratory failure. Acute Respiratory Distress Syndrome occurs frequently in this group, requiring ventilatory support.
Acute kidney injury may accompany sepsis and is in part related to hypotension and partly to the septic insult. Oliguria is an early sign and adequate resuscitation may not always completely reverse this. In about 5% oliguria progresses to anuric renal failure and a period of renal replacement therapy (RRT) is required. Continuous haemofiltration or intermittent haemodialysis are the two most commonly employed modes of RRT in sepsis. Renal function often recovers when the episode of sepsis has resolved.
Sepsis Associated Encephalopathy
Cerebral dysfunction can manifest as confusion, agitation or coma. It is an early sign, often present before other signs of organ failure.
Prolongation of prothrombin and activated partial thromboplastin time, low platelets and deficiencies of protein C, antithrombin 3 or tissue factor pathway inhibitor may be present in sepsis. If severe, disseminated intravascular coagulation may ensue. It is likely that coagulation and fibrin deposition in the microcirculation plays a role in the development of organ failure.
Gut and Liver Dysfunction
Ileus, bowel dysfunction and bacterial translocation may occur as a result of sepsis. Biochemical evidence of liver dysfunction is often seen and reduced liver function may result in reduced lactate clearance.
C-reactive protein, procalcitonin, protein C and IL-6 levels have all been proposed as biochemical markers for sepsis. At present their usefulness is limited and role in management is yet to be clearly defined.