Simplified Edinburgh and modified Boston criteria in relation to amyloid PET for lobar intracerebral hemorrhage.

BACKGROUND: Histopathological evidence of cerebral vascular amyloid ß accumulation is the gold standard to diagnose cerebral amyloid angiopathy (CAA). Neuroimaging findings obtained with CT and MRI can suggest the presence of CAA when histopathology is lacking. We explored the role of amyloid PET in patients with lobar intracerebral hemorrhage (ICH) as this may provide molecular evidence for CAA as well. METHODS: In this retrospective, monocenter analysis, we included consecutive patients with non-traumatic lobar ICH who had undergone amyloid PET. We categorized patients according to amyloid PET status and compared demographics and neuroimaging findings. We calculated sensitivity and specificity of the simplified Edinburgh criteria and amyloid PET with probable modified Boston criteria as reference standard, as well as sensitivity and specificity of the simplified Edinburgh and modified Boston criteria with amyloid PET status as molecular marker for presence or absence of CAA. RESULTS: We included 38 patients of whom 24 (63%) were amyloid PET positive. Amyloid PET positive patients were older at presentation (p = 0.004). We observed no difference in prevalence of subarachnoid hemorrhages, fingerlike projections or microbleeds between both groups, but cortical superficial siderosis (p = 0.003) was more frequent in the amyloid PET positive group. In 5 out of 38 patients (13%), the modified Boston criteria were not fulfilled due to young age or concomitant vitamin K antagonist use with INR > 3.0. With the modified Boston criteria as reference standard, there was no difference in sensitivity nor specificity between the simplified Edinburgh criteria and amyloid PET status. With amyloid PET status as reference standard, there was also no difference in sensitivity nor specificity between the simplified Edinburgh and modified Boston criteria. CONCLUSIONS: Amyloid PET was positive in 63% of lobar ICH patients. Under certain circumstances, patients might not be diagnosed with probable CAA according to the modified Boston criteria and in these cases, amyloid PET may be useful. Accuracy to predict CAA based on amyloid PET status did not differ between the simplified Edinburgh and modified Boston criteria.

Spinal anesthesia in a patient on monoclonal antibody treatment: a poisoned chalice? A case report.

BACKGROUND: Paraplegia is a rare complication of spinal anesthesia. CASE PRESENTATION: We report a case of a 68-year-old man who developed postoperative paraplegia and hypoesthesia after spinal anesthesia for an otherwise uncomplicated transurethral resection of the prostate. Acute transverse myelitis was diagnosed based on urgent MRI. A prior history of similar though less severe neurological symptoms after obinutuzumab treatment for follicular lymphoma suggested a potential causative role for obinutuzumab, a novel monoclonal antibody that has not been associated with such devastating neurological side effects yet. High-dose steroid treatment partially attenuated the symptoms, but debilitating hypoesthesia and motor deficit remained present 3 months postoperatively. CONCLUSION: The presented case warrants caution when performing neuraxial anesthesia in patients on monoclonal antibody therapies.

Non-Lethal Intoxication by Ingestion of 50 Castor Beans: Serial Measurement of Ricinine in Blood, Plasma and Urine.

A 30-year-old woman presented to the emergency department 2 days after ingestion of 50 castor beans. Her symptoms on admission were vomiting, diarrhea, abdominal cramps, agitation and anxiety. Initial laboratory tests showed a slightly elevated C-reactive protein and mild liver and kidney dysfunction. The patient was transferred to the medium care unit of our hospital where she was observed for possible organ failure. During the next days, the kidney function improved and liver function started to recover. Four days after admission, the patient was transferred to the psychiatric ward. Urine, serum, plasma and whole-blood samples were analyzed for ricinine using a quantitative LC-MS-MS method. Initial values on admission (serum and urine) were very high in comparison with previously reported cases. Based on these values, the patient was monitored closely in the following days. The patient made a full recovery, and during the course of hospitalization, concentrations of ricinine in plasma/serum, blood and urine gradually declined. The presence of ricinine in a patient's blood or plasma is a proof of castor bean and, hence, ricin exposure. However, based on this case and previously reported cases in literature, we can conclude that no clear correlation can be established between ricinine blood, plasma or urine levels and the severity of the intoxication. Clinicians should be aware of the potential danger of a ricin intoxication, and patients should be monitored closely for several days due to the unpredictable outcome of the intoxication.