Vasospasm and delayed cerebral ischaemia in patients with spontaneous subarachnoid haemorrhage (aneurysmal and pretruncal non-aneurysmal): a centre’s perspective

@#Spontaneous subarachnoid haemorrhage (SAH) is a significant cause of stroke and may lead to severe neurological deficit or death. It is also associated with high morbidity and mortality for patients despite optimal medical and surgical treatment. Based on the World Health Organization the annual incidence of spontaneous SAH varies in different regions of the world between 2.0-22.5 per 100,000 populations with Finland and Japan having the highest incidence and South and Central America with lowest incidence.1

Oral ketamine induced pathological changes of the urinary tract in a rat model

In recent years, prolonged ketamine abuse has been reported to cause urinary tract damage. However, there is little information on the pathological effects of ketamine from oral administration. We aimed to study the effects of oral ketamine on the urinary tract and the reversibility of these changes after cessation of ketamine intake. Methods: Rats were fed with illicit (a concoction of street ketamine) ketamine in doses of 100 (N=12), or 300 mg/kg (N=12) for four weeks. Half of the rats were sacrificed after the 4-week feeding for necropsy. The remaining rats were taken off ketamine for 8 weeks to allow for any potential recovery of pathological changes before being sacrificed for necropsy. Histopathological examination was performed on the kidney and urinary bladder. Results: Submucosal bladder inflammation was seen in 67% of the rats fed with 300 mg/kg illicit ketamine. No bladder inflammation was observed in the control and 100 mg/kg illicit ketamine groups. Renal changes, such as interstitial nephritis and papillary necrosis, were observed in rats given illicit ketamine. After ketamine cessation, no inflammation was observed in the bladder of all rats. However, renal inflammation remained in 60% of the rats given illicit ketamine. No dose-effect relationship was established between oral ketamine and changes in the kidneys. Conclusion: Oral ketamine caused pathological changes in the urinary tract, similar to that described in exposure to parenteral ketamine. The changes in the urinary bladder were reversible after short-term exposure.