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Myocardial injury in meningococcus-induced purpura fulminans in children
G Briassoulis1, M Narlioglou, N Zavras
1Pediatric Intensive Care Unit, Aghia Sophia Children's Hospital, Athens, Greece. briassg@otenet.gr
Insights
Myocardial ischemia is common in pediatric meningococcemia, indicated by elevated cardiac troponin I (cTnI). High cTnI levels correlate with coagulopathy and impaired heart function, suggesting a need for early intervention.
Area of Science:
- Pediatric Cardiology
- Infectious Diseases
- Critical Care Medicine
Background:
- Meningococcemia can lead to severe complications, including purpura fulminans.
- Myocardial involvement in pediatric meningococcemia is not well-characterized.
Purpose of the Study:
- To determine the incidence of myocardial ischemia in pediatric patients with meningococcus-induced purpura fulminans.
- To correlate cardiac troponin I (cTnI) levels with electrocardiogram (ECG) changes, myocardial function, and coagulopathy.
- To evaluate the relationship between cTnI and disease severity.
Main Methods:
- Studied 22 pediatric patients with acute meningococcemia requiring inotropic or vasoactive support.
- Daily monitoring of serum cTnI, myocardial ischemia markers, and coagulopathy markers.
- Daily measurements of cardiac index, ejection fraction, shortening fraction, and ECGs.
Main Results:
- Five patients (23%) presented with myocardial ischemia, characterized by elevated cTnI levels and depressed myocardial contractility.
- High cTnI levels correlated significantly with low levels of protein C, factor VIII, and antithrombin III.
- Myocardial ischemia was not associated with clinical prognostic scores or inotropic support.
Conclusions:
- Myocardial ischemia is increased in pediatric acute meningococcemia and linked to myocardial dysfunction.
- Elevated cTnI indicates severe coagulopathy but not necessarily poor prognosis based on clinical scores.
- Early detection of myocardial injury and prompt replacement therapy may improve outcomes.
Objectives:
To assess the incidence of myocardial ischemia in meningococcus-induced purpura fulminans in pediatric patients, to compare troponin I (cTnI) levels with changes in electrocardiogram (ECG) and to evaluate whether cTnI is related to myocardial function and contractility, to severe acquired anticoagulant deficiency and to the severity of disease.
Methods:
Twenty-two patients with acute meningococcemia, supported with inotropes or vasoactive agents, were studied, Blood samples for the determination of serum cTnI and conventional myocardial ischemia and coagulopathy markers were drawn daily. Measurements of cardiac index (CI), ejection (EF) and shortening fractions (SF) and ECGs were performed daily.
Results:
The Leclerc score, the Neisseria sepsis index (NESI) and the pediatric risk of mortality (PRISM) score predicted a mean mortality rate of 34%, 27% and 23%, respectively. Four patients died (18%). Five patients (23 %) presented with myocardial ischemia. Their ECG ischemic changes were associated with pathologically high cTnI levels (1.93 +/- 0.13 vs 0.18 +/- 0.08 ng/ml, p < 0.001 for patients with or without ischemic changes) and depressed myocardial contractility (mean difference +/- SE -14 +/- 5%, p = 0.01, for the EF and -7.4 +/- 3, p < 0.02, for the SF). High cTnI values were significantly correlated to low protein C (PC) (p < 0.0001), factor VIII (p < 0.04) and antithrombin III (AIII, p = 0.01) levels, but not to the PRISM, Leclerc or the NESI scores. Means of AIII, VII, and especially of VIII, and PC, were significantly lower in ischemic than in non-ischemic patients, although severity scoring systems and inotropic support did not differ between the two groups. Survivors tended to significantly higher PC (p < 0.01) and factor VIII levels (p = 0.001) than non-survivors and, also, to lower levels of cTnI (p = 0.05) and CPK-MB (p < 0.05), while in meningococcal shock.
Conclusions:
The incidence of myocardial ischemia is increased in acute meningococcemia in pediatric patients and correlates with myocardial dysfunction. High cTnI is associated with severe coagulopathy, but not with clinical prognostic scores or inotropic support. Early recognition of myocardial injury, myocardial support and early replacement therapy with PC, AIII, factor VIII or fibrinogen might improve outcome in acute meningococcemia in children.
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