Intracranial pressure (ICP) was measured in six patients following cardiopulmonary resuscitation (CPR). The causes of cardiac arrest were respiratory or circulatory problems and the primary intracranial pathology was not detected. The measurement of ICP started 3 to 10 h following CPR except one patient in whom it started on the day 7. Duration of ICP measurement ranged from 2 to 7 days. In five out of six patients, ICP persistently remained below 20 mmHg. In the remaining one patient, ICP elevation associated with seizure activity was observed and ICP ultimately increased to 57 mmHg. Among these, four patients died and two remained in a persistent vegetative state. These results suggest that ICP following CPR does not necessarily increase if the patient has no primary intracranial pathology or seizures.

The MIVS technique allowed earlier postoperative recovery with comparable morbidity and mortality rates with the conventional technique and, therefore, saved hospital stay length and total hospitalization charges. Thus, the MIVS technique is considered as a new and effective minimally invasive technique for open AAA repair.

Surgicel, an absorbable haemostat, is widely used in cardiovascular surgery. An 81-year-old woman, who was diagnosed with ischaemic mitral regurgitation, underwent mitral valve plasty and coronary artery bypass grafting. On postoperative day two, her superior vena cava (SVC) pressure gradually rose to 38 mmHg and she developed low output syndrome. Emergent surgery revealed that the cause of SVC syndrome was external compression from a haematoma at the posterior surface of the SVC, which formed around the Surgicel.

No abstract

The reactivity of cerebral blood vessels to changes in Paco 2 in areas of the cerebral cortex with or without diaschisis was investigated in 13 patients in a subacute or chronic stage after a small capsular infarct. A focal area of hypoperfusion (area of diaschisis) was detected in the ipsilateral sensorimotor cortex in each patient. Hyperventilation caused a significant reduction of regional cerebral blood flow in the area without diaschisis and only a tendency for regional cerebral blood flow to decrease in the area with diaschisis; CO 2 inhalation induced a slight increase in regional cerebral blood flow in the area without diaschisis and a significant increase in regional cerebral blood flow in the area with diaschisis. Regional cerebral blood flow reactivity to hypocapnia was significantly less in the area with diaschisis than in the area without, whereas the hypercapnic response was more marked in the area with diaschisis than in the area without. Our results suggest that in the area with diaschisis, the arterioles may be abnormally vasoconstricted at rest such that they cannot constrict further in response to hypocapnia but can dilate more during hypercapnia than in the area without diaschisis. This excessive resting vasoconstriction may result from decreased tissue elaboration of CO 2 due to local decrease of metabolic function. Supported in part by a grant from the Daiwa Health Foundation, Tokyo, Japan.Address for correspondence: Dr. Takashi Takano, Takano Clinic, Tsukamoto 5-6-17, Yodogawa-ku, Osaka, 532, Japan.Received September 4, 1986; accepted March 4, 1988. In the last decade, the use of positron emission tomography (PET) to study stroke has confirmed the original observation relating to diaschisis. Several studies 9 -'' have investigated the relations among blood flow, oxygen metabolism, and glucose utilization and have demonstrated the proportional and parallel reductions in CBF and metabolism in the hemisphere or cerebellum contralateral to that in which diaschisis is manifested. Only a few reports 1213 have described the characteristics of the cerebral blood vessels in the area of diaschisis. The cerebral vascular tone or resistance and the vascular response to changes in mean arterial blood pressure (MABP) or arterial carbon dioxide tension (Paco 2 ) remain unclear.In our preliminary study, 14 we reported on the cerebral vascular tone in the ipsilateral cerebral cortex, in which a small infarct in the internal capsule manifested a focal area of hypoperfusion. The purpose of our current study is to investigate the reactivity of cerebral blood vessels to Paco 2 changes in areas of the cerebral cortex both with and without diaschisis, which result from a small, deep capsular infarct.