inamasu joji

BACKGROUND: For cardiac arrest (CA) victims, brain computed tomography (CT) may serve as a prognosticator. Loss of gray-white matter discrimination (GWMD) and sulcal edema/effacement are reliable CT signs of hypoxia, and a time window may exist for development of these signs. Most data are derived from CA victims of cardiac etiology, however, and CT signs have rarely been evaluated in victims of CA secondary to subarachnoid hemorrhage (SAH). METHODS: A retrospective study was conducted to clarify the incidence, temporal profile, and prognostic significance of early CT signs in resuscitated SAH-CA patients. RESULTS: During a 6-year period, 35 SAH-CA patients were identified. CT signs were observed in 94 %: loss of GWMD was observed in 94 %, whereas sulcal edema/effacement was observed in 77 %. In 29 patients, the interval between CA and the return of spontaneous circulation (ROSC) was estimated. CT signs developed almost invariably when the CA-ROSC interval exceeded 10 min. Loss of GWMD always preceded sulcal edema/effacement. None of the 35 patients achieved long-term survival, regardless of the presence of the CT signs. CONCLUSION: CT signs may develop earlier in patients with SAH-CA than CA of cardiac origin. Because of a poor prognosis, early CT signs are not useful prognosticators in that population.

A case of reversible pontine ischemia following diagnostic cerebral angiography performed to evaluate vertebral artery dissection (VAD) of ischemic onset is reported. A 40-year-old man presented with sudden neck pain, dizziness, difficulty in swallowing, and numbness in the left arm. Neurologically, his symptoms were compatible with incomplete Wallenberg syndrome. Diffusion-weighted magnetic resonance imaging (DWI) revealed a small infarction in the medulla oblongata, and the right VA was irregularly stenotic on magnetic resonance angiography (MRA). We suspected that the right VAD was the cause of the medullary infarction. Following conservative treatment, his deficits resolved quickly despite progression of the VAD as revealed by follow-up MRA. Subsequently, diagnostic cerebral angiography was performed with the purpose of evaluating the patency of the right VA and possibility of a dissecting aneurysm. Despite a seemingly uneventful procedure, however, the patient developed altered mental status and right-sided hemiparesis shortly after the placement of an angiographic catheter into the intact left VA. DWI obtained two hours after the procedure revealed a high-intensity signal in the paramedian pons. Following administration of IV heparin and edaravone, the neurological deficits as well as the high-intensity signal disappeared within 24 h. The patient was discharged without deficits 4 weeks after onset. Although cerebral angiography has been considered the gold standard for the diagnosis of VAD, its role in VAD of ischemic onset has recently been questioned, in light of its relatively benign natural history, improved quality of less invasive imaging modalities, and risks of cerebral angiography. From the perspective of avoiding complications, the common practice of obtaining diagnostic cerebral angiography from every patient with VAD of ischemic onset may have to be reviewed, and decision to perform cerebral angiography for those who have already been diagnosed with less invasive imaging modalities should be made cautiously and on case-by-case basis.

Objects: Recently, several forensic researchers have reported that ketone bodies in body fluids collected postmortem are useful markers for the diagnosis of antemortem ketosis. We measured serum levels of 3-hydroxybutyrate (3-HB), obtained from patients who experienced cardiopulmonary arrest (CPA), and evaluated the relationship between the presumptive causes of CPA and levels of 3-HB.<BR>Material and methods: Between January and April 2008, 125 cases of non-traumatic out-of-hospital CPA were treated at our institution. Levels of 3-HB were measured in 69 of 125 cases to investigate the possible association between ketoacidosis and causes of CPA. The 69 cases were classified into 4 groups based on the serum level of 3-HB, and the frequency of cases having one or more pathophysiological conditions compatible with elevated ketone bodies, namely, a poorly- nourished state, hyperglycemia, or an infectious disease, was calculated. Fifty-eight cases of out-of-hospital CPA with an intrinsic cause were divided into two subgroups depending on whether symptoms prior to CPA were present or not. Accidental-Episodes (AE) group, in which symptoms prior to CPA were absent, consisted of 32 cases. Non-AE group, in which symptoms prior to CPA were present, consisted of 26 cases.<BR>Results: Among the 69 cases assessed, 19 (28%) showed pathophysiological conditions compatible with elevated ketone bodies. The frequency of pathophysiological conditions compatible with elevated ketone bodies was 100% (5 in 5) in cases with 3-HB >1,000 μmol/l, 86% (6 in 7) in cases with 3-HB between 200 and 1,000 μmol/l, 22% (6 in 27) in cases with 3-HB between 50 and 200 μmol/l, and 7% (2 in 30) in cases with 3-HB <50 μmol/l. Among the 58 cases of out-of-hospital CPA with an intrinsic cause, non-AE group had a significantly higher level of 3-HB compared with AE group (p=0.001).<BR>Conclusion: When the serum level of 3-HB is elevated in patients who present with out-of-hospital CPA, it can be speculated that pathophysiological condition compatible with elevated ketone bodies may have been present immediately before their collapse.