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Myocardial dysfunction in children with acute meningococcemia
Insights
Acute meningococcemia can cause myocardial dysfunction, impacting cardiac output. Early detection and treatment of impaired heart function are crucial for survival in affected children.
Area of Science:
- Pediatrics
- Cardiology
- Infectious Diseases
Background:
- Acute meningococcemia often leads to cardiovascular collapse of unknown origin.
- Myocardial dysfunction is suspected in children with this condition.
Purpose of the Study:
- To prospectively assess myocardial function in children with acute meningococcemia.
- To determine the relationship between myocardial function and clinical outcomes.
Main Methods:
- Clinical assessment and echocardiography were used to evaluate myocardial function.
- Left ventricular shortening fraction (LVSF) was measured.
- Cardiac output was assessed using thermodilution.
Main Results:
- 58% of children showed echocardiographic evidence of myocardial dysfunction (depressed LVSF).
- Depressed LVSF correlated with reduced cardiac output.
- Myocardial dysfunction was associated with increased mortality and preceded cardiovascular collapse in some cases.
Conclusions:
- Impaired myocardial function is common in acute meningococcemia and contributes to low cardiac output.
- Assessing myocardial function (LVSF) is vital for guiding therapy and improving survival.
- Therapeutic strategies should consider optimizing myocardial contractility alongside fluid resuscitation.
Abstract:
Acute meningococcemia is frequently associated with cardiovascular collapse of uncertain cause. Review of the records of 12 consecutive children revealed clinical evidence of myocardial dysfunction in six (50%). Subsequently myocardial function was prospectively assessed clinically and echocardiographically in 12 children. Seven (58%) of the 12 children had echocardiographic evidence of myocardial dysfunction as defined by a depressed left ventricular shortening fraction (LVSF). The mean LVSF in these seven children was 0.25 +/- 0.03, as compared with the mean LVSF of 0.39 +/- 0.7 in the remaining children. The LVSF estimate of myocardial function strongly correlated with cardiac output as measured by standard thermodilution (r = 0.98, P less than 0.01). Acute meningococcemia was not fatal in those children without evidence of myocardial dysfunction. In contrast, three of the seven children with evidence of myocardial dysfunction died. In four children, echocardiographic evidence of left ventricular dysfunction preceded cardiovascular collapse and clinical recognition of myocardial dysfunction. In children with an initially low LVSF, recovery of LVSF was associated with survival. Children with acute meningococcemia may have impaired myocardial function as indicated by depressed LVSF, resulting in low cardiac output despite normal intravascular volume. Thus, in addition to restoring intravascular volume, knowledge of the status of myocardial function may help direct therapy toward optimizing myocardial contractility.