**20. Nephrotic syndrome**

Nephrotic syndrome is a known condition which increases the tendency to thrombosis [71, 72]. Although the mechanism of the tendency to thrombosis is not completely known, it is thought that lipid abnormalities increase the tendency to thrombosis by increasing haemoconcentration and hypervolemia and the viscosity of full blood and plasma and that hypoalbuminemia stimulates the synthesis of fibronectin, fibrinogen and factors II, V, X, XI, from the liver [73].

**23. Treatment**

suspected MI [10, 23].

**24.1. Alteplase**

**24. Fibrinolytic treatment**

tion of high-dose tPA [81].

intravenous thrombus cases [83–86].

As there are no comprehensive studies related to PMI treatment, the treatment principles of adult MI treatments have been adapted for children and have been formed from experience focussed on cases. Treatment must be organised according to the aetiology and clinical status of the patient. To determine arrhythmia or for early intervention when it has been determined, ECG monitorisation should be applied as soon as possible to all patients with

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In recent years, alteplase has become the most widely used fibrinolytic drug in children. The most important reasons for selection are that the half-life is short (approximately 5 mins), it is not antigenic and the effect is fibrin-specific [78]. It is a recombinant tissue plasminogen activator. In literature, there is no standard application related to r-tPA dosage in Paediatric patients. There are different applications in different centres. Nakagawa et al. applied intracoronary tPA at the dose of 200,000 unit/kg (0.34 mg/kg) to a patient with Kawasaki disease who suffered MI, but the patient died [79]. Subsequently, doses of 400,000 unit/kg (0.69 mg/ kg) and 800,000 unit/kg (1.38 mg/kg) intra-coronary tPA were applied to 2 other patients with Kawasaki disease who suffered MI, and the thrombi and cliinical findings of the patients were determined to have recovered without any complications. In addition to the tPA, Nakagawa et al. also administered urokinase infusion to the first and third of these three patients. Tsubata et al. applied a dose of 300,000 unit/kg tPA to an MI patient with Kawasaki disease as 10% of the total dose in bolus form and the remainder with a 1-hour infusion [80]. After 2 days, a dose of 50,000 unit/kg tPA was administered intra -coronary, but only a partial response was obtained in the thrombus. Krendal et al. treated a 7-year old Kawasaki patient with MI with intravenous 700,000 unit/kg tPA and a response was obtained clinically on echo. The success in that case compared to Tsubata et al. was associated with the administra-

In cases of intracardiac thrombus and intravascular thrombose**s,** while some centres have used 0.05–0.5 mg/kg/hr. infusion after 0.3–0.6 mg/kg bolus, other centres have administered infusion of 0.01–0.5 mg/kg/hr. without any loading dose, until the thrombus is resolved (max 96 hrs). This has been used and successful results have been obtained in Paediatric cases, especially in the opening of a central venous catheter and in intracardiac or intra-arterial and

After a loading dose of 0.1 mg/kg/10 mins in neonatal infants, some centres have administered maintenance at 0.3 mg/kg/hr. while others have given a loading dose of 0.7 mg/kg in 30—60 mins followed by 0.2 mg/kg/hr. As the infusion time extends, so the possibility of complications developing increases [82, 83]. Major complications that can develop are intracranial bleeding, epistaxis, melena and hematuria and minor complications may be seen as mucosal bleeding or bleeding from the needle entry site. Therefore, patients must be closely
