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• W2995230127 abstract "We are all aware that people with diabetes frequently have arterial disease. They have venous signs and symptoms too. People with severe diabetic neuropathy and neuropathic ulceration often have markedly dilated veins in their feet and lower legs. On measurement, oxygen concentrations in the blood from these dilated veins were similar to arterial blood, whereas levels from hand veins were low. This strongly suggests arteriovenous shunting in the feet. Blood flows rapidly through stiff atherosclerotic arteries and into the veins limiting oxygen delivery to small peripheral vessels and impairing healing.1 Venous disease contributes to 60–80% of leg ulcers in the general population. Venous ulcers arise from incompetent venous valves and weak calf muscle pumping causing venous stasis and hypertension. ‘The natural history of the disease is of a continuous cycle of healing and breakdown over decades and chronic venous leg ulcers are associated with considerable morbidity and impaired quality of life.’2 Venous ulcers are classically in the lower leg above the medial malleolus, painful (eased on elevation), with sloped edges in areas of oedematous, indurated, warm skin, with dilated veins and skin discolouration, such as brownish haemosiderin deposition. Ulcers in people with diabetes may have venous, arterial, and/or neuropathic causes. Rarer causes include bullosis or necrobiosis diabeticorum. Fully assess everyone with leg ulcers,2 particularly for arterial disease. Compression bandaging, a key treatment for venous ulcers, is contraindicated in severe arterial disease. Stiff arteries found in diabetes may not compress on ankle:brachial pressure index (ABPI) measurement producing falsely reassuring high readings. People with diabetes and leg ulcers should be assessed in a specialist diabetes foot and ulcer service which should supervise management.3 In diabetes, plasma levels of clotting factors increase and fibrinolytic capacity reduces.4 Platelets signalling pathways are abnormal with greater activation, adhesion, and aggregation.5 So clots are more likely to form and less likely to break down. In addition, people with diabetes who are hyperglycaemic or ill become dehydrated and often have lower limb problems or other comorbidities. Thus one might expect having diabetes to be a risk factor for venous thromboembolism (VTE). A meta-analysis including 21 studies and 63,552 patients compared people with cardiovascular risk factors with controls. Odds ratios for the risk of VTE were: for obesity 2.33 (95% CI, 1.68–3.24), for hypertension 1.51 (1.23–1.85), for diabetes 1.42 (1.12–1.77), for smoking 1.18 (0.95–1.46), and for hypercholesterolaemia 1.16 (0.67–2.02).6 A large American study analysed 92,240,000 patients with diabetes discharged from hospital from 1979–2005 among whom 1,267,000 (1.4%) had VTE. Relative risk for VTE was greater for patients <50 years old than in older people, with the highest risk in those aged 20–29 years (relative risk 1.73). There was no difference between those with type 1 and type 2 diabetes. Older people did not have an increased risk of VTE.7 In the Nurses’ Health Study, diabetes did not appear to be related to pulmonary embolism.8 The (male) Physicians’ Health Study found that having diabetes increased the risk of coronary heart disease and stroke, but not of VTE. VTE was associated with greater BMI.9 In one population-based US study, having diabetes was a risk factor for VTE; OR 1.47 (1.18–1.84). Accounting for age and obesity attenuated the risk which was no longer increased after also adjusting for hospitalisation with or without surgery and/or nursing home confinement (59.7% of those with diabetes and 14.8% of people without diabetes).10 So, does diabetes increase the risk of VTE? Much of the increased risk shown in some studies appears to be from comorbidities commonly found in people with diabetes, especially those admitted to hospital. So the practical position is to consider everyone with diabetes in hospital for thromboprophylaxis if there are no contraindications. The Department of Health Risk Assessment tool recommended by NICE includes ‘One or more significant medical comorbidities (eg heart disease; metabolic, endocrine or respiratory pathologies; acute infectious diseases; inflammatory conditions)’ as thrombosis risk factors.11 A 21-year-old man with type 1 diabetes and a history of ‘poor control’ was admitted with diabetic ketoacidosis (DKA). He developed multiple venous thromboses including renal, pulmonary, and iliac veins. ‘Hypercoaguability work-up was negative.’12 Forensic pathologists described seven cases of fatal massive pulmonary embolus in DKA. In four patients the diagnosis was made post-mortem.13 While both conditions cause dehydration and thus risk VTE, the substantial fluid loss in hyperosmolar hyperglycaemic state (HHS) is most likely to cause a hypercoaguable state with an increased risk of both arterial and venous thromboembolism. A 60-year-old man was admitted unconscious with ‘hyperosmolar non-ketotic diabetic coma’ and died. ‘At necropsy the mesenteric artery was thrombosed, the entire jejunum and the upper third of the ileum were infarcted…There was embolic obstruction of the right pulmonary artery.’ A 53-year-old man admitted semi-conscious with abdominal symptoms and ‘hyperosmolar non-ketotic diabetic state’ also died from mesenteric infarction.14 National guidance for HHS is that ‘All patients should receive prophylactic low molecular weight heparin (LMWH) for the full duration of admission unless contraindicated.’ Full anticoagulation has been suggested but the guidance does not recommend this.15 Consider extending prophylaxis beyond the duration of admission in patients deemed to be at high risk as one study found that there was a substantially increased risk of VTE during three months after hospital admission for people with diabetes and hyperosmolarity (HR 16.3 [10.4–25.4]). There was an increased risk of post-discharge VTE in people with diabetes without complication (5.2 [3.4–8.1]) and among those who had had DKA (6.8 [4.5–10.3]). ‘The overall incidence of VTE among patients with hyperosmolarity was 1.7%, with 71% of the cases diagnosed during the index hospitalisation, and 29% diagnosed during the 3 months after hospital discharge.’16 Retinal vein occlusion occurs when a retinal vein is blocked by thrombus. It may involve central or branch retinal veins. Retinal vein occlusion causes sudden, painless reduction in vision. It is common, occurring mostly in older people with comorbidities. Hypertension, diabetes, and hyperlipidaemia are the most common risk factors. For example, in one case-control study of people with central retinal vein occlusion 16% had diabetes compared with 9% of controls.17 Central retinal vein occlusion causes macular oedema which may lead to permanent visual loss so the condition should be diagnosed and treated promptly. Untreated it can lead to painful rubeosis with glaucoma. The macular oedema is treated by photocoagulation, intravitreal steroids, or, increasingly, by intravitreal anti-VEGF.18 People with advanced renal disease may need haemodialysis via an arteriovenous fistula in the arm. People with renal disease, especially those with diabetes, have many blood tests and often need intravenous therapy. Every venous puncture causes damage which may be slow to heal. One low renal clearance clinic found that 69% of patients were unaware of the need to preserve veins, and 97% of those who were aware did not practise this. Astonishingly, 99% of health care staff were unaware of the need to protect veins in these patients. They produce information cards. An American site uses wrist bands on the non-dominant arm.20 In people with diabetic foot disease, dilated foot veins may indicate arteriovenous shunting. People with diabetes with venous leg ulcers require specialist assessment, particularly in view of the risk of both arterial and venous disease and complex management. Studies assessing the risk of VTE among people with diabetes have produced mixed results. However, people with diabetes usually have other risk factors for VTE and the consensus is that those in hospital should receive thromboprophylaxis unless this is contraindicated. HHS (and to a lesser extent, diabetic ketoacidosis) is associated with an increased risk of arterial and/or venous thrombosis which may prove fatal. Prescribe thromboprophylaxis unless this is contraindicated. Consider continuing longer-term prophylaxis in people with HHS. Urgently refer anyone with sudden visual loss. Retinal vein occlusion is more common among people with diabetes than in the general population. Protect arm veins in people with renal disease likely to require haemodialysis." @default.
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• W2995230127 date "2019-11-01" @default.
• W2995230127 modified "2023-09-28" @default.
• W2995230127 title "Veins, venous thromboembolism, and diabetes" @default.
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