In a retrospective study conducted in an Italian tertiary care hospital, the incidence of nosocomial candidemia was evaluated together with causative pathogens, treatment, and risk factors for death. Over a 6-year period (1992-1997), a total of 189 episodes of candidemia occurred in 189 patients (mean age 58+/-19 years), accounting for an average incidence of 1.14 episodes per 10,000 patient-days per year. The most common reasons for hospitalization were solid neoplasia (21%), trauma (17%), abdominal diseases requiring surgery (13%), and cardiovascular diseases (13%). No patient was neutropenic within 3 weeks prior to the onset of candidemia. One hundred thirty patients were hospitalized in intensive care units, 47 patients in surgical wards, and 12 patients in medical wards. Candida albicans was the most frequently isolated pathogen, accounting for 54% of fungal isolates, followed by Candida parapsilosis (23%), Candida glabrata (7%), Candida tropicalis (5%), Candida pelliculosa (4%), Candida lusitaniae (1%), Candida humicula (1%), and other non-albicans Candida spp. (5%). Seventy-six (41%) patients received adequate antifungal therapy. Seventy-one (58%) of the 123 evaluable patients with central venous catheters underwent line removal; 51 of them had catheter-related candidemia. The 30-day crude mortality rate was 45%. Older age, hospitalization in an intensive care unit, a longer duration of candidemia, retention of central lines, and inadequate antifungal therapy were significantly associated with poor outcome. In the present study, nosocomial candidemia was a frequent and relatively underestimated illness. Adequate antifungal therapy and central line removal independently reduced the high mortality of the disease.

4 cases of spontaneous disappearance of intracranial arteriovenous malformations are reported. All the malformations were in the rolandic-parietal area, and fed in most cases by the MCA. In one case, the malformation was associated with a proximal aneurysm. One malformation was large, one medium-sized, and two small. Venous drainage was towards the longitudinal sinus in all cases. Presenting symptoms consisted of epilepsy in 2 cases, and intracerebral haemorrhage in 2 cases. Disappearance of the AVM was documented by angiography from 1 to 15 years after diagnosis, and was preceded by a new haemorrhage in 2 cases. Acute or gradual thrombosis of the AVM is suggested as the most likely cause of the disappearance of an AVM. Spontaneous thrombosis of an AVM should be considered as an aspect of the pathological entity known as "thrombosed AVM". Guidelines for the management of patients exhibiting spontaneous disappearance of an AVM are briefly discussed.

Cerebral vasospasm occurs frequently after head injury. Correlation between neurological deterioration and vasospasm has been reported previously, but delayed neurological deterioration secondary to vasospasm in head injury is a rare occurrence. We report the case of a 57-year-old man who, after a motorcycle accident, developed an acute subdural hematoma and a thick subarachnoid deposition of blood in the left sylvian-insular cistern. After surgical evacuation of the hematoma, the patient improved until the 10th postoperative day, when he developed aphasia and a right hemiparesis. Angiography demonstrated multitapering spasm, and a computed tomographic (CT) scan showed persistence of the cisternal deposition of blood. Despite therapy with hypervolemia, the patient improved only slightly. The association of head injury with substantial subarachnoid hemorrhage producing vasospasm has been considered rarely. Delayed posttraumatic vasospasm secondary to blood degradation products seems to play some role in the vasospasm after head injury. CT scanning may be useful in predicting vasospasm in such patients, and digital subtraction angiography might be useful in demonstrating it.

Cerebral vasospasm occurs frequently after head injury. Correlation between neurological deterioration and vasospasm has been reported previously, but delayed neurological deterioration secondary to vasospasm in head injury is a rare occurrence. We report the case of a 57-year-old man who, after a motorcycle accident, developed an acute subdural hematoma and a thick subarachnoid deposition of blood in the left sylvian-insular cistern. After surgical evacuation of the hematoma, the patient improved until the 10th postoperative day, when he developed aphasia and a right hemiparesis. Angiography demonstrated multitapering spasm, and a computed tomographic (CT) scan showed persistence of the cisternal deposition of blood. Despite therapy with hypervolemia, the patient improved only slightly. The association of head injury with substantial subarachnoid hemorrhage producing vasospasm has been considered rarely. Delayed posttraumatic vasospasm secondary to blood degradation products seems to play some role in the vasospasm after head injury. CT scanning may be useful in predicting vasospasm in such patients, and digital subtraction angiography might be useful in demonstrating it.

On the whole, these data demonstrate the early onset of oxygen radical-mediated oxidative stress, proposing a valid explanation for the failure of clinical trials based on the administration of oxygen free radical scavenger drugs and suggesting a possible rationale for testing the efficacy of lipid peroxidation "chain breakers" in future clinical trials.