Purpose of review
The underlying pathophysiology of sepsis has long been disputed. Systemic vasodilatation is important in the development of shock and, in septic critically ill adults who have been volume resuscitated, the systemic pressure is often low and the cardiac output high. In septic children however, and especially in those with meningococcal septic shock
, poor cardiac output as a consequence of depressed myocardial function seems to be important, often being the cause of death in these patients. There is much evidence for disturbance of myocardial performance, yet despite the literature, there is still no consensus on how best to manage this complication of meningococcal disease
Many mediators have been proposed as the cause of the reduced myocardial performance, most recently interleukin-6 has emerged as a possible candidate involved in the pathophysiology of the myocardial dysfunction. Cardiac troponin I has been shown to be a marker of myocardial injury and may be used to monitor left ventricular function. Newer treatments emerging to manage the dysfunction include reports of success with phosphodiesterase inhibitors.
Accepting that myocardial dysfunction may be an important cause of the shock state in overwhelming meningococcal disease
, the approach to management may need to be tailored appropriately. Although presently there is no targeted treatment, it may be that therapy focused on inhibiting or antagonising interleukin-6 will be helpful in the future. Regardless of the importance of myocardial depression, fluid resuscitation remains a cornerstone in the management of severe meningococcal disease