Vomiting, headache and seizures in a child with idiopathic nephrotic syndrome.

to phenprocoumon and this was continued for 4 Case report months. Treatment with prednisone, albumin and furosemide A 5-year-old patient with idiopathic nephrotic synresulted in complete remission of the nephrotic syndrome had been successfully treated with a course of drome. Two years later the patient is free of neurologsteroids. Four months later the patient had a first ical residues. relapse of the nephrotic syndrome, which was also steroid responsive. Three weeks after the second course of steroid treatment, while still receiving 40 mg/m2/day Discussion prednisone, the child was admitted because of frequent vomiting and headache. Physical examination of the Patients with a nephrotic syndrome are at increased child was normal except for peripheral oedema. risk of venous and arterial thrombosis. This includes Neurological investigation was unremarkable. Blood cerebral venous thrombosis, although this complication pressure was 125/80 mmHg. Laboratory results has not been frequently reported [1]. A number of included the following: leukocytes 30 200/ml, haemofactors predispose to thrombosis: apart from altered globin 14.4 g/dl, haematocrit 47%, platelet count procoagulatory factors (particularly low antith306 000 ml, total protein 4.4 g/dl, creatinine 0.37 mg/dl. rombin III ), altered fibrinolytic factors and abnormal Lp(a) level on admission was 750 mg/dl (reference platelet aggregation, some potentially avoidable factors range <300 mg/l ). Urinary protein excretion was may also be present, e.g. intravascular volume deple1.5 g/24 h. tion with haemoconcentration. Of particular interest is Since headaches were present without signs of hyperthe potential relation between elevated Lp(a) in the tension, a cranial computed tomography was performed. It showed a so-called ‘empty triangle sign’, indicating a cerebral venous thrombosis (Fig. 1). Following the CT scan the patient suddenly developed a left-sided seizure of approximately 45 min duration. This could only be stopped by i.v. administration of phenobarbital and phenytoin. The seizure was followed by a transient left-sided hemiparesis. Treatment of cerebral venous thrombosis was started immediately with i.v. administration of heparin (240–350 U/kg/day). In addition, acetylsalicylic acid (4 mg/kg/day) and substitution with antithrombin III was provided. A control CT on the following day revealed two small parasagittal areas of parenchymal intracerebral haemorrhage in the right parietal lobe. Follow-up cranial CT scans demonstrated complete resorption of cerebral haemorrhage and total resolution of cerebral venous thrombosis after 3 weeks. Four weeks later the patient was switched from heparin