Sepsis is a complex, multifactorial syndrome which can evolve into conditions of varying severity. If left untreated, it may lead to the functional impairment of one or more vital organs or systems. Therefore its adequate treatment is crucial already in emergency room.
Early detection and timely therapeutic intervention in emergency room can improve the overall clinical outcome of septic patients; reducing time to diagnosis of sepsis is thought to be a critical component in reducing mortality from multiple organ failure.
It is well known that early treatment with aggressive haemodynamic support can limit the damage of sepsis-induced tissue hypoxia and prevent the over stimulation of endothelial activity.
Early, adequate hemodynamic support of patients in shock is crucial to prevent worsening organ dysfunction and failure.
Fluid therapy to improve microvascular blood flow and increase cardiac output is an essential part of the treatment of sepsis.
A fluid challenge incorporates four determinant elements:
- crystalloid solutions should be the first choice, because they are well tolerated and cheap,
- fluids should be infused rapidly to induce a quick response but not so fast that an artificial stress response develops,
- the goal should be an increase in systemic arterial pressure, and
- pulmonary edema is the most serious complication of fluid infusion.
Hypotension is the most common indicator of inadequate perfusion and restoring a mean systemic arterial pressure of 65 to 70 mm Hg is a good initial goal during the haemodynamic support of patients with sepsis.
Haemodynamic resuscitation has been the cornerstone of management of patients with sepsis and septic shock in SSC guidelines since its first draft.
However, in patients with abdominal sepsis, requiring urgent surgical intervention, overly aggressive fluid resuscitation may increase intra-abdominal pressure and worsen the inflammatory response, which is associated with a high risk of complications
In patients with generalized peritonitis, fluid resuscitation should be kept under control to avoid fluids overload, which may aggravate gut oedema and lead to increased intra-abdominal pressure. Increasing intra-abdominal pressure causes progressive hypoperfusion of splanchnic circulation. The frequency with which intra-abdominal hypertension develops in abdominal sepsis may have other important clinical consequences in addition to its impact on sepsis resuscitation endpoints.
Moreover, pathophysiological effects include gut oedema leading to bacterial translocation and release of cytokines, therefore aggravating the sepsis cascade
Vasopressor agents should be administered to restore organ perfusion if fluid resuscitation fails optimizing blood flow in various organs.
Vasopressor agents should be administered early in patients with sepsis or septic shock of abdominal origin to restore organ perfusion. Their early use may prevent excessive fluid resuscitation.
Norepinephrine is now the first-line vasopressor agent used to correct hypotension in the event of septic shock. It is more efficacious than dopamine and may be more effective for reversing hypotension in patients with septic shock. Moreover dopamine may cause more tachycardia and may be more arrhythmogenic than norepinephrine,
Dobutamine is the an inotropic agent used for increasing cardiac output, regardless of whether norepinephrine is also being given. With predominantly β-adrenergic properties, dobutamine is less likely to induce tachycardia than isoproterenol.
Increased global availability of vasopressors together with a better understanding of their indications, pharmacodynamics, and important adverse effects are mandatory to fight sepsis worldwide.