Consent obtained by the junior house officer--is it informed?

Of 30 junior house officers questioned, 21 had obtained patients' consent for colonoscopy. Of these 21, about one-third did not routinely discuss with patients the risks of perforation and haemorrhage. Ideally, consent should be obtained by a person capable of performing the procedure. If it is to be obtained by junior house officers, they need to know exactly what must be disclosed about each procedure. This could easily be done as part of the induction package.

Does venous function deteriorate in patients waiting for varicose vein surgery?

We have looked at the deterioration in the condition of the lower limbs in a group of 36 patients who were waiting for a median time of 20 months for varicose vein surgery, using clinical examination, colour Duplex scanning and photoplethysmograph (95% refilling times). We found a significant deterioration in this group of patients, with four limbs initially unaffected developing reflux on Duplex scanning, of which three had clinical varicose veins (all four were offered surgery), and of the initial 56 involved limbs, 10 further sources of reflux were found (18%), necessitating alteration of the initial planned surgical procedure. No patient developed deep venous insufficiency or ulceration while on the waiting list, although there was one new case of lipodermatosclerosis. However, had surgery been undertaken after the first assessment, 14 patients (25%) would potentially have required further surgery, although accepting this as justification for allowing patients to wait takes no account of patients suffering or quality of life while waiting for operation.

Randomised clinical trial of the duration of compression therapy after varicose vein surgery.

OBJECTIVE: To determine whether a period of one or three weeks of compression following varicose vein surgery influenced the outcome. DESIGN: Randomised controlled trial. METHOD: 300 patients aged between 18-80 years underwent unilateral varicose vein surgery in a Day Procedure Unit. Compression bandaging was applied post-operatively for three days. Patients then wore graduated elastic compression stockings randomised to a period of either one or three weeks. Patients were assessed by questionnaire on pain scores at rest and during mobilisation for up to six weeks, total analgesic consumption, duration of time off work, any complications, and patient perception of cosmetic results at various periods up to 12 weeks following surgery. RESULTS: The mean pain score reported by patients over 6 weeks was similar in the two groups (1 week group: mean 2.18, three week group: mean 1.87). The 95% confidence interval (CI) for the mean difference in pain was (-0.05-0.66). Analysis of the pain curves at 1 week, 4 weeks and 6 weeks, showed equivalence at 4 and 6 weeks, but not for 1 week, with the group wearing stockings for only one week complaining of more pain for this period. A significant increase in the total number of analgesia tablets consumed was also found in the group wearing stockings for only one week. No significant differences were found in the other secondary endpoints - return to work (categorised as <2 weeks, 2-6 weeks or 6-12 weeks), patient satisfaction or post-operative complications. CONCLUSION: We found no benefit in wearing compression stockings for more than one week following uncomplicated high saphenous ligation with stripping of the great saphenous vein with respect to post-operative pain, number of complications, time to return to work, or patient satisfaction for up to 12 weeks following surgery.

Treatment of the critically ischaemic lower limb.

Medical therapy of PAOD is only indicated in patients unsuitable for vascular reconstruction or angioplasty. The approach includes early detection of subjects at risk, avoidance of known risk factors, and appropriate management of diseases such as diabetes and hypertension. Vasodilators are of little use orally, though some drugs may have a part to play for short-term management and iloprost should be considered for patients unsuitable for revascularization. The ankle systolic or toe pressure should be used as a measure of disease and, if reduced, arteriography should be performed. This should not be limited to those thought fit for major surgery, as angioplasty or thrombolytic therapy may be appropriate, and aortoiliac disease may be treated by extra-anatomic bypass if not suitable for major surgery. Arterial reconstruction is associated with a reduction in both mortality and amputation, and should be attempted if a greater than 25% chance of limb salvage could be expected.

Thrombolysis in acute lower limb ischaemia.

For the past three decades balloon embolectomy has been the treatment of choice for acute lower limb occlusion. However, although usually successful in emboli, results are often disappointing in thrombotic atherosclerotic vessels. Attempted dissolution of the clot is accordingly attractive, and has theoretically been possible since the introduction of streptokinase in 1933. This was initially used intravenously, with variable success rates, although intraarterial administration is currently the method of choice. Later thrombolytic drugs such as tissue plasminogen activator, urokinase and anistreplase have been introduced. Lysis time has also been increased by using pharmaco-mechanical methods of administration such as pulsed spray catheters, which could increase the usefulness of thrombolysis in patients with rapidly progressive neurological signs where currently surgical embolectomy would be advocated. Several newer drugs with theoretical advantages over older drugs such as single-chain urokinase-type plasminogen activator or K1K2PU are currently undergoing trials. The role of thrombolysis as an adjunct to surgical embolectomy is also promising, though again requires further trials. There is still no consensus as to which patients are best suited to thrombolysis, nor an optimum drug or method of administration. However, there seems no doubt that thrombolysis will be increasingly used in the management of peripheral limb ischaemia, though requiring a team approach between surgeons, radiologists and haematologists.

Leukocyte migration in the leg in response to experimental venous hypertension.

PURPOSE: Leukocyte trapping and activation in the microcirculation of the legs may play an important role in causing skin damage in venous disease. Leukocyte emigration from the microcirculation and subsequent locomotion in response to venous hypertension was studied in a group of 12 normal volunteers using a "skin window" technique. METHODS: Two 0.5-cm square dermal abrasions were made with a dental stone over the gaiter area of the leg and the flexor aspect of the forearm (control), which were covered with moist micropore membranes. The volunteers lay supine for 30 minutes, and then stood supported for 30 minutes to raise the venous pressure in the leg, and then lay supine again for 30 minutes. The experiment was repeated in six volunteers who lay supine for the whole period. The membranes were changed and collected every 15 minutes, fixed in formal saline solution, and dual-stained for monocytes and polymorphonuclear leukocytes. The type and numbers of cells that emigrated and the furthest distance traveled (leading front) by the cells through the membrane were measured. RESULTS: Both in arms and legs, the vast majority of cells that emigrated were neutrophils, with very few monocytes (arm, 93% neutrophils and 7% monocytes; leg, 97% neutrophils and 3% monocytes). In the 30 minutes after venous hypertension, leukocyte migration significantly decreased in the leg (median leukocyte locomotion: basal, 75.3 microns; standing, 73.5 microns; after hypertension, 62.9 microns; p = 0.012, Wilcoxon matched pairs signed rank test), but not in the arm (basal, 86.2 microns; standing, 84.4 microns; after hypertension, 85.5 microns; p = NS) or when the experiment was repeated with the volunteers lying supine for the entire period (basal, 91.5 microns; standing, 89.4 microns; after hypertension, 92.6 microns; p = NS). CONCLUSIONS: Leukocyte migration is decreased immediately after experimental venous hypertension, which may be a result of the release of factors that inhibit migration.

Selection of amputation level: a review.

Preservation of the knee joint in a patient undergoing lower limb amputation for critical ischaemia is associated with improved postoperative rehabilitation and mobility. Yet, for most surgeons the below-knee to above-knee amputation ratio remains less than one. Poor wound healing and a high reamputation rate for below knee stumps are important factors mitigating against below-knee amputations. Many tests (Doppler indices, segmental pressures, skin blood flow, skin perfusion pressure, TcpO2, thermography) have been described to predict the likelihood of successful healing of an amputation stump but none appears to have gained widespread acceptance. Clinical judgement alone is insufficient to predict the success or failure of an amputation stump. In this review, we have looked at the evidence in support of these tests, particularly those routinely available to most surgeons.

Leg ulceration in venous disease.

We have given a brief summary of the scale of the problem caused by venous ulceration in the UK, and have then reviewed the various theories of causation, including a historical survey, and presented the evidence for and against the two main current theories of fibrin cuffs and white cell trapping. We also outline previous hypotheses of the aetiology of venous ulceration, including arteriovenous microanastomoses, stasis and oedema. The contribution of superficial venous incompetence in the pathogenesis of ulceration is also examined.

Photoplethysmography: a valuable noninvasive tool in the assessment of venous dysfunction?

We have investigated the photoplethysmography findings in 152 patients admitted to the Middlesex Hospital Vascular Laboratory with suspected lower limb venous disease, and we compared the results obtained with patient grouping using clinical criteria and the presence of reflux on color duplex scanning. All photoplethysmography traces were normalized with use of computer software to enable direct comparison between the traces. The parameters investigated were the 95% and 50% refilling times and the initial gradient of the refilling curve. Receiver operating characteristic curves were constructed to determine which parameter was the most useful predictor of disease and to identify which value within each observation gave the greatest sensitivity and specificity. We found a large overlap between interquartile values for all three parameters, with limbs grouped both clinically and by duplex scanning, making differentiation between normal and abnormal limbs difficult on the basis of photoplethysmography traces alone. We found that a 95% refilling time of less than 15 seconds indicated venous dysfunction with the greatest sensitivity and specificity and suggest that this value is most useful. Photoplethysmography readings are reproducible, noninvasive, and correlate well with the presence of clinical disease, and photoplethysmography remains useful in the assessment of venous dysfunction.

Peripheral nerve function in chronic venous insufficiency.

Abnormalities of vasomotion, impairment of the venoarteriolar reflex and increased skin blood flow reported in the liposclerotic skin of patients with chronic venous insufficiency (CVI) suggest altered nervous control of the skin microcirculation. The aim of this study was to determine whether patients with CVI have a peripheral neuropathy. Forty patients with CVI and lipodermatosclerosis (LDS) and 35 age and sex-matched controls were examined for neuropathy using three modalities of testing. Threshold to warming was used to assess unmyelinated fibres, and threshold to cooling and vibration to assess myelinated fibres. Warming and cooling thresholds were measured on the sole of the foot by a purpose built, computer controlled instrument. The threshold to vibration was measured on the big toe using the Ohio Bio-thesiometer. A significantly raised threshold to warming and vibration was found in the CVI group compared to the normal controls [median threshold to warming (interquartile range) in CVI group = 5.3 (0.1-9.1) median threshold to warming (interquartile range) in controls = 1.21 (0.17-3.5), p = 0.005 and median threshold to vibration (interquartile range) in CVI group = 22 (13-31) median threshold to vibration (interquartile range) in controls = 12 (8.5-27.5), p = 0.024]. The thresholds to cooling was not statistically different in the two groups. This study demonstrates the presence of a peripheral neuropathy in patients with chronic venous insufficiency, and this may be important in the pathogenesis of venous ulceration.

Plasma elastase in venous disease.

The plasma elastase level was measured as a marker of neutrophil degranulation in three groups, each of 15 patients, with uncomplicated varicose veins, lipodermatosclerosis (LDS) and venous ulceration. The values obtained were compared with those in age- and sex-matched control subjects. Significantly higher levels of elastase were found in all patient groups compared with controls: median 25.6 ng/ml for patients with uncomplicated varicose veins, 22.1 ng/ml for those with LDS, 26.0 ng/ml for those with venous ulceration. There was no difference in neutrophil count between the patient and control groups. These results provide evidence of increased neutrophil degranulation in patients with venous disease. The finding of raised elastase levels in all three patient groups shows that this was not due solely to the inflammatory process characterizing LDS and venous ulceration.

Leukocyte activity in the microcirculation of the leg in patients with chronic venous disease.

PURPOSE: It has been suggested that leukocyte trapping and activation in the microcirculation of the leg skin causes lipodermatosclerosis and ulceration in patients with chronic venous disease. Ambulatory venous hypertension is accepted as the physiologic factor that leads to ulceration. We investigated leukocyte endothelial adhesion in patients who were subjected to short-term venous hypertension. METHODS: Two groups of patients with venous disease were studied: group 1, varicose veins with skin changes (n = 15); and group 2, varicose veins without skin changes (n = 15). Blood samples were taken from a foot vein before and after standing for 30 minutes to raise the venous pressure in the lower limb, and after lying supine again for 10 minutes. The samples were analyzed for leukocyte surface CD11b and L-selectin (CD62L) expression using a flow cytometer. Plasma-soluble L-selectin was also measured using an enzyme-linked immunosorbent assay. RESULTS: In patients with skin changes, median neutrophil CD11b levels fell from 4.66 to 3.83 arbitrary units (p = 0.005, Wilcoxon) after 30 minutes of venous hypertension, Median monocyte CD11b levels fell from 7.65 to 5.8 arbitrary units (p = NS, Wilcoxon) after venous hypertension and then fell further to 5.43 arbitrary units (p = 0.02 vs baseline; Wilcoxon) when the venous hypertension was removed. Neutrophil and monocyte L-selectin levels also fell in response to venous hypertension, remaining low even after venous hypertension was removed. A similar pattern was seen in patients with uncomplicated varicose veins. There was a rise in soluble L-selectin in the plasma of both groups of patients after venous hypertension, reflecting leukocyte adhesion to endothelium. In the group of patients with skin changes the level of soluble L-selectin rose from 695 ng/ml to 836 ng/ml (p = 0.02, Wilcoxon), and in the group without skin changes the rise was from 700 ng/ml to 801 ng/ml (p = 0.02, Wilcoxon). CONCLUSION: Venous hypertension results in sequestration of the more activated population of neutrophils and monocytes in the microcirculation of the leg in patients with venous disease. These cells bind to the endothelium, releasing L-selectin, and do not emerge from the limb when venous hypertension is reversed. These findings do not differ between patients with varicose veins and those with skin changes.

Endothelial activation in patients with chronic venous disease.

OBJECTIVES: Leukocyte trapping due to leukocyte-endothelial activation has been implicated as the cause of lipodermatosclerosis and ulceration in patients with chronic venous disease. We investigated endothelial activity in normal controls and patients subjected to short-term venous hypertension. METHODS: Twenty-five normal volunteers and 30 patients with chronic venous disease divided into two groups: varicose veins with skin changes (LDS, n = 15); and varicose veins without skin changes (VVs, n = 15) were studied. Blood samples were taken from a foot vein before and after experimental venous hypertension. Plasma levels of ELAM-1 (endothelial leukocyte adhesion molecule-1), ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1), and von Willebrand factor (vWf) was measured by an ELISA. RESULTS: There was a significant rise in the plasma concentration of ELAM-1, ICAM-1 and VCAM-1 in patients and normal controls in response to venous hypertension. Basal levels of plasma VCAM-1 and vWf were higher in patients with LDS compared to patients with VVs. The magnitude of rise of VCAM-1 was greater in patients with LDS compared to patients with VVs (p = 0.01, Mann-Whitney U-test). There was no difference in the basal levels or in the magnitude of change in plasma ICAM-1 and ELAM-1 between the two patient groups. CONCLUSION: Venous hypertension results in endothelial activation which may aid endothelial-leukocyte adhesion. Patients with LDS exhibit increased VCAM-1, which is a counterligand for receptors expressed by monocytes and lymphocytes signifying that these cells may be more important in the development of skin changes.