Recurrence of Kikuchi's lymphadenitis after 12 years.

A 40 year old woman developed recurrent Kikuchi's disease 12 years after the original episode. The recurrence affected the same site (axilla) and occurred after the longest delay so far recorded in a European resident. Care must be taken to avoid misdiagnosis of Kikuchi's disease as lymphoma.

Management of co-existing intra-abdominal disease in aortic surgery.

OBJECTIVES: the treatment of abdominal aortic aneurysms more than 5 cm in diameter is well accepted, but controversy surrounds the management of concomitant serious intra-abdominal lesions diagnosed in the perioperative period. This study was undertaken to demonstrate that synchronous surgery is feasible and safe in this group of patients. DESIGN: in 1978 a decision was made to undertake combined operations on all patients with an aortic aneurysm of 5 cm or more in diameter and a significant non-vascular intra-abdominal lesion requiring surgery. METHODS: the case records of 676 patients who had aortic grafting for aneurysmal disease or the urgent management of occlusive disease between 1978 and 1998 were analysed retrospectively. SETTING: district general hospital. RESULTS: fifty-six (8%) patients had co-existing intra-abdominal disease treated at the time of aortic graft surgery. There were three (5%) hospital deaths and seven patients required early reoperation. One patient developed a subphrenic abscess and there were three superficial wound infections. There has been no clinical evidence of aortic graft infection in this series. CONCLUSION: this single centre experience with synchronous surgery demonstrates that it is safe and does not appear to predispose to an increased risk of graft infection.

Microembolism from aortic aneurysm and ventricular thrombus: a complication of intravenous streptokinase.

Two patients sustained the rare complication of skin infarction following administration of intravenous streptokinase for acute myocardial infarction. We report evidence that dissolution of thrombus from an unsuspected source and subsequent microembolization of the skin may be responsible for this complication. In patients known to have an aortic aneurysm or ventricular thrombus, careful consideration should be given to the use of intravenous streptokinase following myocardial infarction.

Calcium channel blockade in rats with cyclosporine-induced vasoconstriction.

Calcium channel blockade has been found to attenuate nephrotoxicity of cyclosporine. However, it is not known whether intrarenal vasoconstriction caused by cyclosporine is totally mediated by vascular smooth muscle calcium influx. To study the protective effects of two calcium blockers on cyclosporine-induced intrarenal vasoconstriction and renal microvascular blood flow, hydronephrotic rat kidneys were suspended in an environmentally controlled tissue bath. Renal microvessel diameters and microvascular blood flow were determined by in vivo videomicroscopy and Doppler velocimetry. Calcium channel blockade was achieved by adding verapamil hydrochloride (5.6 x 10(-5) M) or diltiazem hydrochloride (2.8 x 10(-5) M) to the tissue bath, which respectively resulted in a 15 +/- 2% and 16 +/- 3% interlobular arteriolar dilation, a 13 +/- 3% and 12 +/- 2% afferent arteriolar dilation, and a 60 +/- 8% and 46 +/- 14% increase in interlobular blood flow. When cyclosporine (1.7 x 10(-3) M) was added to the tissue bath, there was a constriction of the interlobular arterioles to 4 +/- 3% below baseline in rats receiving verapamil and 9 +/- 3% below baseline in rats receiving diltiazem. Microvascular blood flow was reduced by the addition of cyclosporine to 3 +/- 4% above original baseline values in the verapamil group and 22 +/- 6% below baseline in the diltiazem group. Afferent arterioles were similarly constricted by cyclosporine. The results indicate that calcium blockade causes preglomerular vasodilation and protects the microvascular blood flow induced by cyclosporine. Since verapamil or diltiazem did not prevent arteriolar constriction as observed when cyclosporine was added, it was concluded that the mechanism of acute cyclosporine-induced vasoconstriction is not solely mediated by vascular smooth muscle calcium influx through potential dependent channels.

In vivo assessment by videomicroscopy of acute renal microvascular responses to cyclosporin.

Nephrotoxicity limits the use of cyclosporin A for immunosuppression after organ transplantation and may be caused by glomerular hypoperfusion. Indirect studies have shown that cyclosporin A increases renal vascular resistance and reduces total renal blood flow. This study used direct in vivo videomicroscopy to define the effects of the drug on the renal microcirculation of the rat. An intravenous infusion of cyclosporin A (20 mg per kg body-weight) caused a 13 per cent acute constriction of the proximal interlobular artery and an associated 29 per cent reduction in preglomerular interlobular arterial blood flow. There was a simultaneous increase in mean arterial blood pressure of 34 per cent caused by cyclosporin A and a 23 per cent increase in systemic vascular resistance. Cyclosporin acutely reduces renal microvascular blood flow by vasoconstriction and affects the central circulation, suggesting that a generalized peripheral vasoconstriction is induced.

Risk factors and operative mortality in surgery for colorectal cancer.

The operative mortality rate after surgery for colorectal carcinoma remains significant. A series of 578 patients has been studied prospectively. The features which most significantly affect operative mortality are the age of the patient, a history of loss of weight, limited preoperative patient mobility and the presence of intestinal obstruction with perforation of the bowel. By identifying high-risk groups of patients, attention may be focused on particular patients at risk, in order to reduce operative mortality.

The role of intrarenal prostaglandins and angiotensin II in acute cyclosporine-induced vasoconstriction.

Cyclosporine causes intrarenal vasoconstriction, which may account for its nephrotoxic effects. In this study we investigated the role of endogenous prostaglandins and angiotensin II in cyclosporine-induced intrarenal vasoconstriction. Split hydronephrotic kidneys in decerebrate rats (n = 16) were suspended in an environmentally controlled tissue bath. Interlobular, afferent, and efferent arteriolar diameters and red blood cell velocity were measured by in vivo video-microscopy and Doppler velocimetry. After topical application of cyclosporine to the kidney in the tissue bath, a 12% +/- 2% constriction of the interlobular and a 28% +/- 5% reduction in interlobular blood flow occurred. The afferent and efferent arterioles also constricted by 13% +/- 2% and 10% +/- 3%, respectively. Prostaglandin inhibition with mefenemate augmented this vasoconstriction (16% +/- 2% at interlobular and 21% +/- 4% at afferent arterioles) and reduction in interlobular blood flow (38% +/- 8%) below baseline values. Mefenemate alone resulted in a 35% +/- 5% reduction in interlobular blood flow, which was not further augmented by cyclosporine. In contrast, local competitive angiotensin II-receptor inhibition with saralasin maintained blood flow after cyclosporine and prevented intrarenal vasoconstriction by cyclosporine. This suggests that prostaglandins protect against intrarenal vasoconstriction and that acute cyclosporine-induced vasoconstriction is mediated through angiotensin II receptors.

The influence of the cyclosporine vehicle, cremophor EL, on renal microvascular blood flow in the rat.

Cyclosporine nephrotoxicity may be due to glomerular hypoperfusion. Previous experimental and clinical studies have demonstrated a decrease in renal blood flow and an increase in renal vascular resistance. Cremophor EL, which is the vehicle in which CsA is dissolved, is thought to be a factor involved in intrarenal arteriolar vasoconstriction. To determine the relative contributions of the vehicle and CsA to intrarenal arteriolar vasoconstriction, we used in vivo videomicroscopy and Doppler velocimetry to measure changes in renal microvascular blood flow in the rat. A 5-min intravenous infusion of 20 mg/kg of CsA resulted in a 17% mean reduction (P less than 0.05) in the diameter of preglomerular interlobular arterioles and an associated 60% reduction (P less than 0.05) in microvascular blood flow by 15 min. Cremophor EL/ethanol equivalent caused less vasoconstriction (up to 10%) but resulted in a 42% mean decrease (P less than 0.05) in microvascular blood flow, probably secondary to a 38% mean decrease (P less than 0.05) in cardiac output and 13% decrease in arterial pressure. We conclude that cremophor EL does contribute to in vivo reduction of preglomerular microvascular blood flow in the rat. This may be particularly important when using this intravenous preparation in the study of CsA nephrotoxicity.

Ulnar artery aneurysms after injury mimicking acute infection in the hand.

Two cases of ulnar artery aneurysm, with concomitant ulnar nerve compression in the palm are presented. Both followed acute injury and presented with an increasingly painful, warm swelling within 2 weeks of injury. An initial diagnosis of infection was made by experienced clinicians in each case. Ulnar artery aneurysm may be wrongly diagnosed as acute infection. It is suggested that simple excision of the aneurysm and ligation of the ulnar artery is the treatment of choice. Angiography should be reserved for those cases where there is doubt about the diagnosis or adequacy of the collateral circulation. Ulnar nerve deficit may be a result of direct injury rather than a neuropraxia from compression by the aneurysm.