Plasma-exchange treatment for severe carbamazepine intoxication: a case study.

Acute poisoning is an important cause of morbidity and mortality during childhood. This manuscript reports the positive outcome of a pediatric case with a history of accidental carbamazepine intake treated using plasma exchange. A 3-year-old male presented with severe carbamazepine intoxication. He was comatose and had generalized tonic clonic seizure, ventricular tachycardia, and hypotension. Although he did not respond to classical therapies, we performed two sessions of plasma exchange. The patient recovered rapidly and was discharged from the hospital six days from the time of carbamazepine ingestion with no complication or neurologic impairment. Plasma exchange can be performed safely in very small children, and it might be the first line treatment, particularly for intoxication with drugs that have high plasma-protein-binding properties.

Hemispheric cerebrovascular venous thrombosis due to closed head injury.

CASE REPORT: We present the case of an 8-month-old infant who was admitted to our Neurosurgery Department with venous infarction related to sagittal sinus thrombosis. The infarction was radiologically detected 5 days after the baby had undergone surgery for acute subdural hematoma due to a closed head injury. RESULTS AND CONCLUSIONS: Cerebrovascular venous thrombosis is a rare clinical entity that has multiple causes and variable presenting symptoms. There is no consensus on overall strategy concerning surgical, radiosurgical, or medical therapy (anti-coagulation, thrombolytic, and anti-edema treatment), and exactly how, when, or in which cases these should be applied. The treatment planning should be based on clinical findings, and should be modified according to the clinical course. In this case, the clinical and radiological findings regressed with symptomatic treatment alone.

Acute disseminated encephalomyelitis associated with hepatitis A virus infection.

We describe the case of a 30-month-old boy who developed acute disseminated encephalomyelitis (ADEM) after hepatitis A virus (HAV) infection and ultimately died. As far as we know, this is only the second case of HAV-associated ADEM to be reported in the literature. The child was brought to hospital with fever, lethargy and weakness of 2 days duration. He had developed jaundice, abdominal pain and malaise 2 weeks beforehand and these problems had resolved within 2 days. Neurological examination revealed lethargy, generalised weakness and positive Babinski's signs bilaterally. Cerebrospinal fluid examination showed mild lymphocytic pleocytosis, increased protein and elevated anti-HAV IgM and IgG titres. Serum HAV IgM and IgG titres were also elevated. Despite aggressive treatment with ceftriaxone, acyclovir and anti-oedema measures, he developed papilloedema and coma within 24 hours of admission. Magnetic resonance imaging of the brain revealed diffuse cerebral oedema and multifocal hyperintensities on T2-weighted images, with most lesions in the white matter of both cerebral hemispheres. The diagnosis of ADEM was established and high-dose steroids and intravenous immunoglobulin were added to the treatment regimen. However, his clinical condition continued to deteriorate and he died on the 20th day in hospital. This case shows that HAV infection can be linked with ADEM. Patients with HAV infection should be examined carefully for central nervous system symptoms during follow-up. Likewise, the possibility of HAV infection should be investigated in cases of ADEM.