Thrombolysis in fulminant menigococcemia (FM) with myocardial infarction (MI) and shock

A 15-year-old boy presented with fever, confusion, headache and nausea. On examination, he had purpuric lesions, meningeal irritation and signs of systemic inflammatory response to sepsis. Cultures were obtained and ceftriaxone was administered. Laboratory findings were consistent with impending disseminated intravascular coagulation (DIC) and the patient was given fresh frozen plasma (FFP), antithrombin III (AT III) and low dose enoxaprin. Hemodynamics improved with fluid challenge. However, 12 hours later, he became agitated and developed shock. The patient was intubated and given high doses of catecholamines. The ECG and the echocardiogram showed extensive acute anterior wall MI. We decided to perform thrombolysis with recombinant tissue plasminogen activator (t-PA) given over 4 hours (total dose 1.25 mg/kg) [1]. Shortly after thrombolysis, hemodynamics improved and the ECG normalized. Peak CPK levels were 5200 IU/ml. The patient developed multiple organ failure (MOF) with adult respiratory distress syndrome and renal failure. Neisseria meningitidis group C was found in the cerebrospinal fluid. The patient recovered completely afterwards. The followup echocardiogram showed normal left ventricular function and mild anterior hypokinesis.

FM, or Waterhouse Friderichsen syndrome, is characterized by the abrupt development of shock, DIC and MOF. Impaired myocardial contractility is commonly seen in FM and contributing to shock. It is well established that endotoxin causes myocardial dysfunction [1] and plays a key role in septic myocardial dysfunction. The exact mechanisms of endotoxine-induced myocardial dysfunction are complex and probably involve cytokines such as tumor necrosis factor-α [2, 3] and perhaps also myocardial apoptosis [4]. MI during FM is exceedingly rare, and to our knowledge only one case hase been reported in the pediatric literature [5]. Our patient developed MI, presumably on the basis of DIC, despite aggressive treatment. Although levels of plasminogen activator antigen are increased in septic shock, its activity is almost completely inhibited by plasminogen activator inhibitor type 1 (PAI-1). Theoretically, treatment with t-PA may help reverse the procoagulant state. Zenz et al. [1] and others [6–8] observed significant clinical improvement after a 4-hour infusion of t-PA in a few pediatric patients with FM. This is the first report of successful thrombolysis with t-PA in a patient with FM complicated by MI and shock.