SUMMARY Measurement of intracranial arterial blood flow velocity is a new technique with potentially a number of very useful applications. This study validates the technique by comparing it to cerebral blood flow (CBF) measured using intravenous Xenon and extracranial clearance recording. We have measured the middle cerebral artery (MCA) blood flow velocity in 17 symptomatic patients with the EME TC 264 transcranlal Doppler velocimeter and compared these measurements to the ipsilateral hemispheric cerebral blood flow measured with an intravenous Xenon 133 technique (Novo Cerebrograph 10A). Measurements were made at rest and during hypercapnia.The absolute measurement of MCA velocity and hemispheric CBF showed a poor correlation (r = 0.424, p < 0.01) due to wide between-patient variations at rest but the blood flow response to hypercapnia, expressed as a reactivity index, showed a good correlation (r = 0.849, p < 0.001).Thus changes hi MCA velocity reliably correlate with changes hi cerebral blood flow but the absolute velocity cannot be used as an indicator of CBF.Stroke which has a number of potentially useful applications. It has been advocated as a method of peroperative monitoring during carotid endarterectomy when it can provide continuous on-line information about middle cerebral artery velocity, 2 ' 3 information of particular importance when the common carotid artery is clamped in deciding which patients need shunting.4 It may also be used to predict preoperatively whether or not the use of an indwelling shunt is necessary.3 Another use for the technique has been in the assessment of cerebrovascular spasm following subarachnoid hemorrhage 6 ' 7 and furthermore measurement of blood flow velocity in the middle cerebral artery, anterior cerebral artery and posterior cerebral artery combined with common carotid compression can provide information on the integrity of the Circle of Willis. 8 In an attempt to show that Doppler measured middle cerebral artery velocity corresponds to cerebral blood flow, a number of workers have performed hypercapnia stress tests and measured the resulting increase in middle cerebral artery velocity. "11 However, this only provides indirect proof of the validity of these measurements. Therefore, we have measured the response to hypercapnia of both the middle cerebral artery velocity and the cerebral blood flow measured with an intravenous Xenon 133 technique. A good correlation between the two methods would provide direct evidence that middle cerebral artery velocity changes actually reflect changes in cerebral blood flow. Methods PatientsIn order to get a wide spread of response to hypercapnia, we have studied 17 symptomatic patients with Received December 18, 1985; accepted January 23, 1986. cerebrovascular disease aged between 41 and 70 years (mean 61); providing 34 middle cerebral arteries for study. In 11 instances, the ipsilateral internal carotid artery was totally occluded and in the remaining 23 was patent. Measurement of MCA VelocityThe probe of the EME TC 264 2...

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A series of 45 patients with chylous ascites has been reviewed. The age at presentation ranged from 1 to 80 (median 12) years; 23 patients were aged < or = 15 years. Thirty-five patients had an abnormality of the lymphatics (primary chylous ascites); in the remaining ten, the ascites was secondary to other conditions, principally non-Hodgkin's lymphoma (six patients). Two principal mechanisms of ascites formation were identified using lymphangiography and inspection at laparotomy: leakage from retroperitoneal megalymphatics, usually through a visible lymphoperitoneal fistula (14 patients); and leakage from dilated subserosal lymphatics of the small intestine, invariably associated with leaking lacteals causing protein-losing enteropathy (24 patients). Both sites of leakage were present in a further five patients. In the remaining two patients, chyle was leaking from normal mesenteric lymphatics, in one via a ruptured mesenteric lymph cyst and in the other from the site of a previous lymph node biopsy. Other associated lymphatic abnormalities were present in 36 patients, lymphoedema of the leg being the commonest (26 patients). All patients were initially treated conservatively with dietary manipulation; this was the most satisfactory treatment for those with leaking small bowel lymphatics. Surgery (fistula closure, bowel resection or insertion of a peritoneovenous shunt) was performed in 30 patients. Closure of a retroperitoneal fistula, when present, was the most successful operation, curing seven of the 12 patients so treated.

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Forty-nine patients with the Klippel-Trenaunay syndrome have been studied. Sixty-eight per cent have a superficial, embryological venous channel on the lateral aspect of the limb, 25 per cent have had one or more severe spontaneous haemorrhages from dilated varices and 22 per cent have suffered a venous thrombo-embolism. Twenty-nine per cent have had episodes of rectal bleeding or haematuria associated with pelvic angiomas. Foot volumetry (n = 31) showed that calf emptying was decreased in only five patients and only one of these had phlebographic evidence of deep venous obstruction, which conflicts with previous findings. The rate of calf refilling was increased in 81 per cent and phlebography demonstrated incompetent communicating veins in 45 per cent of patients. No patient had clinical evidence of an arteriovenous fistula, and arteriography (n = 22) and calf blood flow (n = 33) were normal, but lymphangiography (n = 14) showed lymphatic hypoplasia in 55 per cent of limbs. Eighty-eight operations have been performed on 38 patients but symptoms persist in 90 per cent. We suggest that surgery should be limited to the excision of localized symptomatic abnormalities and that the best form of control is provided by graduated compression stockings.