Clinical Features

The following clinical features may be present:

Distributive shock

  • Patients with sepsis are usually warm, flushed and vasodilated.
  • They are frequently hyperdynamic –  tachycardic and hypotensive but with a high cardiac output.
  • There may be signs of reduced tissue perfusion – elevated serum lactate and low central venous oxygen saturation. The rise in lactate seen in sepsis may also 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 shockand so-calledcharacterised 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.

Respiratory failure

  • Tachypnoea is often an early and important sign.
  • As sepsis progresses, pulmonary oedema and metabolic acidosis contribute to progressive hypoxaemia and
  • Acute respiratory distress syndrome occurs frequently in this group, requiring ventilatory support.

Renal dysfunction

  • 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 usually 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.

Haemostatic 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.

Biomarkers

  • C-reactive protein is used routinely as a marker of inflammation. Procalcitonin, protein C and IL-6 levels have all been proposed as biochemical markers for sepsis. At present, their usefulness is limited and their role in management is yet to be clearly defined.