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This meta-analysis was rated fair-quality because it did not adequately describe included trials and used an unvalidated method to measure ‘global response’ buy viagra 25 mg amex erectile dysfunction fix. This study found that the ‘global response’ was equivalent for cyclobenzaprine and diazepam (66% marked or moderate improvement) and significantly better than placebo (40%) discount 100mg viagra erectile dysfunction drugs over the counter canada. Results of head-to-head trials None of the 12 head-to-head trials was rated good-quality; all had at least two important methodological flaws (Evidence Table 5) order viagra line erectile dysfunction systems. All trials were rated fair except one trial of cyclobenzaprine versus diazepam that was rated poor because in addition to other flaws, it 126 only reported results for 52 of the 105 enrollees and did not account for the other patients. Of the fair-quality trials, the trial that appeared to be of best quality compared carisoprodol and 129 diazepam. In this trial the authors did not describe allocation concealment techniques, and they used unvalidated methods for assessing outcomes. Carisoprodol was found to be significantly superior to diazepam using unvalidated methods of stiffness, tension, and relief, with average differences for carisoprodol compared to diazepam averaging about 0. No significant differences were seen for pain, activity impairment, or sleep impairment. In other head-to-head trials, a variety of methods were used for measuring outcomes, including various scales for pain (4, 5, or 9 point scales and visual analogue scales), tenderness, and functional status. Most assessment scales were unvalidated, and methods of reporting these outcomes were inconsistent. Functional status was either not measured or assessed using unstandardized and unvalidated methods. Doses of medications investigated were cyclobenzaprine 10 to 20 mg tid; tizanidine 2 to 8 mg tid, chlorzoxazone 500 mg tid to 750 mg qid, carisoprodol 350 mg qid, and diazepam 5 to10 mg tid (Table 4). In these trials, there was no clear evidence that one skeletal muscle relaxant was superior to any other for 123 efficacy. In a trial comparing tizanidine and chlorzoxazone in patients with back pain, there were no significant differences between treatments for muscle pain, muscle tension, tenderness, and activity. More patients reported ‘excellent’ overall results with tizanidine (57%) compared to chlorzoxazone (23%), but similar proportions of patients reported ‘good or excellent’ results (79% vs. A trial of cyclobenzaprine versus methocarbamol in patients with localized muscle spasm found that there were no significant differences in the proportion Skeletal Muscle Relaxants Page 19 of 237 Final Report Update 2 Drug Effectiveness Review Project of patients reporting absent or mild muscle spasm, limitation of motion, or limitation of daily 20 activities. A slightly greater proportion of patients on cyclobenzaprine reported mild or absent local pain compared to methocarbamol (40% vs. In a trial of cyclobenzaprine versus 124 carisoprodol in patients with acute back pain and spasms there were no significant differences for pain, muscle stiffness, activity impairment, sleep impairment, tension, or relief scores compared to baseline. Other head-to-head trials compared an included skeletal muscle relaxant to diazepam. One other 128 trial reported decreased tenderness, decreased limitation of motion and better ‘global evaluation’ for cyclobenzaprine vs. All three of these trials received funding support from a pharmaceutical manufacturer (Merck) and were published in the same book. For most outcomes that favored cyclobenzaprine, the magnitude of difference between treatments was greater at the end of week one than at the end of week two. In one trial comparing chlorzoxazone to diazepam, chlorzoxazone was superior for unvalidated measures of pain, spasm, tenderness, limitation of 51 motion, and interference with activities. In two trials comparing cyclobenzaprine to 126, 127 130, 131 diazepam and two trials comparing tizanidine to diazepam, no significant differences were found for any clinical outcomes including pain, stiffness, or functional ability. In all head-to-head trials, the overall withdrawal rates ranged from 0% to 35%. In one trial, the overall withdrawal rate 166 167 appeared significantly higher on cyclobenzaprine (12/34 ) compared to diazepam (3/32 ), but there was no significant difference in the withdrawal rate between interventions in other trials. External validity was difficult to assess in these trials, for reasons similar to those described for head-to-head trials in patients with spasticity. Results of placebo-controlled trials None of the 46 placebo-controlled trials (including six head-to-head trials with a placebo arm, one of which evaluated both methocarbamol and cyclobenzaprine versus 20 placebo ) involving patients with musculoskeletal conditions was rated good quality (Evidence Table 6). Quality was generally at the same level or worse than the head-to-head trials. Most of these trials evaluated patients with acute neck or low back conditions, and most showed some evidence for clinical efficacy of evaluated skeletal muscle relaxants, but the magnitude of benefit was difficult to assess because of marked heterogeneity in study design, interventions, populations studied, and outcomes assessed (Table 5). Carisoprodol (four trials), cyclobenzaprine (21 trials), orphenadrine (four trials), metaxalone (five trials), and tizanidine (seven trials) were evaluated in the highest number of trials, and most studies found significant benefits or trends towards benefit on active treatment compared to placebo. A small number of placebo-controlled trials evaluated baclofen (1 trial), methocarbamol (3), and dantrolene (2) for musculoskeletal conditions. Baclofen, dantrolene, and tizanidine are not FDA-approved for Skeletal Muscle Relaxants Page 20 of 237 Final Report Update 2 Drug Effectiveness Review Project use in patients in musculoskeletal conditions. Although trials of baclofen and dantrolene found significant benefits or trend toward benefit from active treatment, the data on metaxalone was 56, 153 mixed. Two fair-quality trials found no differences compared to placebo, but a poor- 43 44 quality trial and two fair-quality trials reported in the same publication did find benefits compared to placebo using unvalidated outcome measures. We identified no placebo- controlled trials evaluating chlorzoxazone. Most placebo-controlled trials evaluated patients with acute back or neck pain, or nonspecified acute muscle spasm. Of five trials that evaluated patients with fibromyalgia, 41, 145 two found that cyclobenzaprine was superior to placebo for at least some measures of 58, 149, 151 sleep quality, fatigue, and pain (Table 5 and Evidence Table 6). The other three found no differences in assessed outcomes. Two randomized controlled trials (n=737 and 668) reported in one publication evaluated the efficacy of different doses of cyclobenzaprine versus placebo (Table 5 and 47 Evidence Table 6). Both trials were short-term (7 days), were rated fair quality for internal validity, and used unvalidated outcomes measures for ‘global impression of change’, ‘medication helpfulness’, ‘relief from starting backache’, and proportion of ‘responders’. One trial evaluated the efficacy and adverse events of cyclobenzaprine 5 mg po tid and 10 mg po tid compared to placebo. It found that the two cyclobenzaprine regimens were roughly equivalent for efficacy for the assessed outcomes. What are the comparative incidence and nature of adverse effects (including addiction and abuse) of different muscle relaxants in patients with a chronic neurologic condition associated with spasticity, or a chronic or acute musculoskeletal condition with or without muscle spasms? Patients with spasticity Summary Reliable data are lacking on comparative adverse event rates from skeletal muscle relaxants in patients with spasticity. In almost all trials evaluated, there was little or no evidence of rigorous adverse event assessment. There is limited fair-quality evidence from eight head-to-head trials that the adverse event profiles of tizanidine and baclofen are different, as most head-to-head trials of these two medications have found that more patients on tizanidine experienced dry mouth while more experienced weakness on baclofen. There was no clear evidence that intolerable adverse events were more frequent with tizanidine compared to baclofen. There was insufficient evidence to judge the comparative safety of other skeletal muscle relaxants in patients with spasticity. Serious side effects appeared rare, but there appears to be a small but significant risk of serious (including fatal) dantrolene-related hepatic Skeletal Muscle Relaxants Page 21 of 237 Final Report Update 2 Drug Effectiveness Review Project injury. Although asymptomatic, reversible elevations of aminotransaminases have been reported with tizanidine, serious or fatal hepatic injury appears extremely rare on this medication. Serious hepatic toxicity has not been associated with baclofen.

Computed tomography–an increasing surveillance CT scans in patients with diffuse large B-cell non- source of radiation exposure generic 75 mg viagra erectile dysfunction drugs india. Five things physicians and patients computed tomography in the follow-up of diffuse large B-cell should question order discount viagra occasional erectile dysfunction causes. Five things physicians and patients follow-up procedures in patients with large-cell lymphoma who should question purchase 100 mg viagra overnight delivery impotence support group. Elis A, Blickstein D, Klein O, Eliav-Ronen R, Manor Y, Lishner 41. Parker A BB, Devereux S, Gatter K, Jack A, Matutes E, et al. Detection of relapse in non-Hodgkin’s lymphoma: role of Best practice in lymphoma diagnosis and reporting. Committee for Standards in Haematology and the Royal College 37. Powell2 1Degenerative Disease Research, Center for Neuroscience, Aging, and Stem Cell Research, Sanford Burnham Medical Research Institute, La Jolla, CA; and 2Division of Hematology and Oncology, University of California Davis Cancer Center, Sacramento, CA Hemophilia is caused by a functional deficiency of one of the coagulation proteins. Therapy for no other group of genetic diseases has seen the progress that has been made for hemophilia over the past 40 years, from a life expectancy in 1970 of 20 years for a boy born with severe hemophilia to essentially a normal life expectancy in 2013 with current prophylaxis therapy. However, these therapies are expensive and require IV infusions 3 to 4 times each week. These are exciting times for hemophilia because several new technologies that promise extended half-lives for factor products, with potential for improvements in quality of life for persons with hemophilia, are in late-phase clinical development. Whereas in vitro clotting of plasma consumed Hemophilia is caused by a functional deficiency of one of the the factor deficient in hemophilia A (FVIII), most of the factor coagulation proteins and can lead to spontaneous internal bleeding, deficient in hemophilia B (FIX) was not consumed. The 2 factors which can result in joint damage, intracranial hemorrhage, and were separated because FIX selectively bound to insoluble barium death. Hemophilia was documented as a sex-linked disorder more salts, which led to the isolation of the proteins for determination of than 1700 years ago in the Talmud. From the protein sequence, described the genetics of hemophilia A as an X chromosome-linked reverse genetics was applied to isolate the human genes in the early bleeding disorder. In 1904, Tsarevich Alexis was born targets for mutation and inactivation. After hemorrhages appeared in Alexis, his mother, Em- Concerns over virus contamination were heightened when individu- press Alexandra, turned to Rasputin, who was reputed to create als receiving pooled plasma-derived products became infected with miracles, for help. Although thought to be the more common factor hepatitis in the 1970s. Then, in the early 1980s, it became apparent VIII (FVIII) deficiency, it was recently found posthumously that that HIV had contaminated the blood supply because the majority of Queen Victoria had factor IX (FIX) deficiency. The disastrous epidemics of viral contamina- The modern era of hemophilia treatment began with the detection of tion prompted the rapid development of recombinant-derived FVIII, FVIII in human plasma in 19115 and the description of its role in with the first 2 products approved by the Food and Drug Administra- hemostasis in 1937. Protein was suitable for storage and use at home in 1968. The availability of replacement therapy has reduced the morbidity, improved the factor replacement led to marked improvement in the life expec- quality of life, and normalized life expectancy. Long-term prophy- tancy of a boy born with severe hemophilia, from 20 years in lactic therapy reduces or prevents the development of hemophilic 1970 to essentially a normal life expectancy today. This article is reprinted with permission from Blood. Protein Name Modification Clinical status* Reference(s) Protein replacement strategies FVIII wt FVIII Pegylated liposomes No increase in T1/2; phase 3 completed 17, 18, 55 N8-GP Single 40 kDa PEG attached to 21 amino Well-tolerated; in phase 3 31 acid B-domain BAX855 2 mol PEG/full-length FVIII 1. In addition, as a mechanism for sustained release did not yield significant convenient access to peripheral veins remains difficult, and many beneficial results in vivo16-17,18 Most recent success has been children require use of central venous access devices, which are achieved by conjugation at specific sites of the factor with polyeth- associated with the medical risks of sepsis and thrombosis. Impor- ylene glycol (PEG), a hydrophilic polymer, or by fusion of the tantly, 25% to 30% of hemophilia A patients and 3% to 4% of factor with the Fc fragment of Ig or albumin. Although these fusion hemophilia B patients develop inhibitory alloantibodies to the approaches have substantially increased the plasma T1/2 of vitamin infused product. This is likely due to different mechanisms of clearance between FIX/FVIIa and FVIII. Previous studies demonstrated that New products in clinical development FIX clearance is likely mediated through interaction of the aminoter- The recent years mark the most revolutionary developments in minal Gla domain residues 3-11 with endothelial/collagen IV sites, although the specific mechanism remains unclear. Since the due to binding to phospholipid surfaces of cells. In the presence of 1/2 development of recombinant-derived products in the 1990s, there VWF, FVIII is stabilized in the plasma to a T1/2 of 12 hours. The has been an ever-growing interest in developing new products clearance of FVIII from the plasma is likely dependent on the through biotechnology to circumvent present limitations for therapy. A variety of approaches have evolved to increase the T1/2 of the proteins in plasma to reduce dosage frequency with the goal of PEGylation reducing cost. In addition, with increased structural and functional PEGylation involves the covalent attachment of PEG to a protein to understanding of the mechanism by which FVIII and FIX exert their improve its therapeutic effect. In the late 1970s, random PEG coagulant activity, specific variants have been engineered with addition was shown to reduce the immunogenicity of proteins. Similar approaches have been applied to most common method of PEG addition is through covalent attach- activated factor VII (FVIIa) for the treatment of patients with ment to lysine residues or N-terminal amines, but this often reduces inhibitory antibodies. These products have the potential for simpler activity of the protein and the extent of PEG addition is variable, prophylactic regimens, obviate the need for central catheters, and producing a heterogeneous product and complicating reliable synthe- possibly improve the quality of life of those afflicted with hemo- sis for consistent effectiveness. This review primarily focuses on those therapeutics that have site-specific PEGylation has significant advantages. More than 10 PEGylated protein therapeutics have been approved for use, including anti-TNF mAb Fab Several approaches have proven successful in increasing the T of fragment,22 VEGF-aptamer, Epoetin , and IFN- 2. There have been modifications to the long-term safety concerns due to the PEGylation have arisen with molecule to reduce proteolytic degradation and modification of the any of the approved therapeutics. Of course, weekly use of Hematology 2013 31 PEGylated FVIII from early childhood may be a somewhat different may limit the inhibitory activity of inhibitory antibodies. Several studies have found that PEGylated proteins in factors that are in clinical development. In hemophilia animal general show reduced immunogenicity compared with their models of bleeding, all of these PEGylated FVIII molecules have unmodified parent molecules. Available safety information of PEGylated proteins A mice and rabbits. However, there are differences in how the PEGylation is unmodified FVIII. Finally, the efficient PEGylation facilitates achieved, and subtle differences may become apparent as the consistent conjugation at a single site, although thorough charac- clinical trials proceed through phase 3. On the Small PEG molecules are more rapidly cleared than large ones. The positive side, production of these site-directed PEGylated FVIIIs rate of excretion is closely related to T1/2. It should be noted that PEG is also present in some not permeate into tissues as well as smaller ones. With 10-kDa plasma-derived FVIII products that have been used in patients PEG, there is increased pinocytotic uptake into macrophages and for many years without safety concerns.

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Incidence of gastrointestinal-related adverse events (diarrhea purchase viagra in united states online erectile dysfunction desi treatment, flatulence cheap viagra 100mg visa candida causes erectile dysfunction, nausea discount viagra 50mg fast delivery erectile dysfunction newsletter, abdominal pain, constipation, gastritis) and angioneurotic edema (1 person in the enalapril group) were not 62 significantly different between the telmisartan and enalapril groups. Neither trial of telmisartan compared with an ACE-I in adults with hypertension reported results of subgroup analyses based on demographics, comorbidities, or concomitant medication use. Comparison of combination therapy with an AIIRA plus an ACE-I to AIIRA and ACE-I monotherapies in adults with hypertension We included 6 trials (in 7 publications) that compared combination therapy with an AIIRA plus 54, 71, 77, 79-82 an ACE-I to AIIRA and ACE-I monotherapy, respectively. Three of these trials were 54, 77, 81, 82 rated poor quality, however, and a detailed analysis of their results will not be provided. Descriptions of the reasons for their poor quality ratings can be found either above in the ‘monotherapy compared with monotherapy’ section or in Evidence Table 5. Among the 71 79, 80 remaining 3 trials, 1 was rated good quality and 2 were rated fair quality. The good-quality trial compared the combination of losartan 50 mg plus ramipril 5 mg to monotherapy with either losartan 50 mg or ramipril 5 mg over 24 weeks in 51 adults who were nondiabetic and had normal renal function, but who were all macro albuminuric (baseline mean albumin excretion 71 rate ranged from 350 mg/24 hours to 460 mg/24 hours). Among the fair-quality trials, 1 compared the combination of valsartan 80 mg plus benazepril 10 mg to monotherapy with either valsartan 80 mg or benazepril 10 mg over 3 months in 90 adults who were nondiabetic with no 79 renal disease, but with microalbuminuria/macroalbuminuria (albumin-to-creatinine ratio). The other fair-quality trial, the VALERIA trial, compared 30 weeks of treatment with a combination of valsartan/lisinopril 320/20 mg to monotherapy with valsartan 320 mg and lisinopril 40 mg in 80 133 adults with hypertension and microalbuminuria. In VALERIA, 73% of participants also had type 2 diabetes. DRIs, AIIRAs, and ACE-Is Page 44 of 144 Final Report Drug Effectiveness Review Project Effectiveness/efficacy outcomes All 3 trials found significantly greater reductions in microalbuminuria levels with AIIRA/ACE-I combination therapy compared with ACE-I monotherapy. Reduction in mean albumin-to- 79, 80 71 creatinine ratio or albumin excretion rate ranged from 52% to 62% for the AIIRA/ACE-I combination groups, compared with a range of 25% to 41% in the ACE-I monotherapy groups. However, compared with valsartan monotherapy, reduction in albumin-to-creatinine ratio was not 80 significantly greater with the combination of valsartan/lisinopril (–51% compared with –62%). None of the trials provided results of formal analyses that ruled out the possibility that the superior reduction in albumin levels in the combination treatment groups could be explained only by differences in blood pressure-lowering effects. But, authors of 1 trial stated that strict 71 blood pressure control protocol used in all treatment groups discounted such a suggestion. There were no significant differences between groups for overall withdrawals in any of the trials. Harms The VALERIA trial (N=133), which compared valsartan/lisinopril combination therapy to 80 monotherapy with valsartan and lisinopril, provided the most extensive reporting on harms. In the VALERIA trial, there were no significant differences between valsartan/lisinopril combination therapy and either valsartan or lisinopril monotherapy groups in overall adverse events (72% compared with 63% or 62%) or withdrawals due to adverse events (8% compared with 7% or 7%). Hypotension was the most frequent adverse event in the valsartan/lisinopril combination therapy group (12%), but the difference as compared to the incidence in the valsartan and the lisinopril monotherapy groups (9% and 2%, respectively) was not statistically significant. There were no withdrawals due to adverse events in the trial that compared 71 losartan/ramipril combination therapy to losartan and ramipril monotherapies. In the trial of valsartan/benazepril combination therapy, the only adverse event-related withdrawals were 2 79 (7%) participants from the benazepril monotherapy group, both owing to severe cough. Subgroups None of the trials involving AIIRA/ACE-I combination therapy in adults with hypertension reported results of subgroup analyses based on demographics, comorbidities, or concomitant medication use. Nondiabetic Chronic Kidney Disease Summary of findings Proteinuric chronic kidney disease: Comparison of monotherapies • Losartan compared with lisinopril (1 trial; fair quality) o Effectiveness/efficacy: A statistically greater reduction in proteinuria was noted for those treated with lisinopril compared with losartan; change in creatinine clearance and blood pressure control were equivalent between groups. DRIs, AIIRAs, and ACE-Is Page 45 of 144 Final Report Drug Effectiveness Review Project o Harms: Dizziness and hyperkalemia were reported by treatment group and rates were numerically similar between groups. No statistically significant differences in decline in creatinine clearance were noted. No significant difference between groups for reduction in proteinuria. No significant difference in creatinine clearance between groups. No significant change in creatinine clearance was noted in either group. No significant difference between groups regarding change in creatinine clearance. There was no statistically significant change in creatinine clearance. No significant difference between groups for change in glomerular filtration rate. Change in creatinine clearance numerically similar pre and post treatment in 1 trial. No significant difference between groups for renal function. Combination therapy with AIIRAs and ACE-Is Combination of ACE-I and AIIRA compared with monotherapy with either agent • Combination therapy losartan plus an ACE-I (4 trials) o Losartan plus lisinopril (1 trial; fair quality): Differential effect for proteinuria reduction was seen favoring combination therapy, but blood pressure control was not equal between groups. There were no statistically significant changes in creatinine clearance between groups. Rates of hyperkalemia and dizziness were numerically greater in combination therapy arm. One trial showed equivalent proteinuria reduction between groups at trial completion. Changes in creatinine clearance were not significantly different between groups. Numerically similar rates of dizziness and hyperkalemia for combination therapy and monotherapy with enalapril; numerically slightly fewer events for losartan monotherapy. No differential effects between groups for changes in creatinine clearance. No significant change in creatinine clearance was seen between groups. The incidence of hyperkalemia was statistically less likely in the candesartan group compared with the combination arm. In the latter study blood pressure control was not equivalent between groups. One trial noted increase in glomerular filtration rate for combination therapy greater than for monotherapy, but creatinine clearance changes were not different between treatment groups. One trial noted no hyperkalemic events in either group. No difference was seen in changes in creatinine clearance between groups. Numerically more participants experienced dizziness in combination arm compared with either monotherapy arm; numerically more participants experienced hyperkalemia in combination arm compared with irbesartan arm. Combination of ACE-I and AIIRA compared with monotherapy with either ACE-I or AIIRA • Combination therapy of an ACE-I and an AIIRA compared with an ACE-I alone (4 trials) o Losartan and lisinopril compared with lisinopril alone (1 trial; fair quality): No differential effects found between groups for proteinuria reduction. Markers for change in renal function were inconsistent; glomerular filtration rate was lower for those on combination therapy but there was no difference between groups in creatinine clearance.

Near its origin it gives rise The posterior tibial artery to medial and lateral circumflex femoral branches viagra 50 mg free shipping erectile dysfunction clinic. These con- • Course: the posterior tibial artery arises as a terminal branch of the tribute to the trochanteric and cruciate anastomoses (see below) generic viagra 50 mg fast delivery best erectile dysfunction pills treatment. It is accompanied by its venae comitantes and supplies The profunda descends deep to adductor longus in the medial com- the flexor compartment of the leg purchase 100mg viagra fast delivery erectile dysfunction in 20s. Approximately midway down the partment of the thigh and gives rise to four perforating branches. These circle the femur posteriorly perforating, and supplying, all The artery ultimately passes behind the medial malleolus to divide into muscles in their path. The profunda and perforating branches ulti- medial and lateral plantar arteries under the flexor retinaculum. The mately anastomose with the genicular branches of the popliteal latter branches gain access to the sole deep to abductor hallucis. Posterior to the medial malleolus the structures which can be identifiedafrom front to backaare: tibialis posterior, flexor digitorum The trochanteric anastomosis longus, posterior tibial artery and venae comitantes, the tibial nerve and This arterial anastomosis is formed by branches from the medial and flexor hallucis longus. It lies close to the trochanteric fossa and pro- • Peroneal arteryathis artery usually arises from the posterior tibial vides branches that ascend the femoral neck beneath the retinacular artery approximately 2. It courses between fibres of the capsule to supply the femoral head. It ends by dividing into a The cruciate anastomosis perforating branch that pierces the interosseous membrane and a This anastomosis constitutes a collateral supply. The deep branch runs • Course: the femoral artery continues as the popliteal artery as it between the 3rd and 4th muscle layers of the sole to continue as the passes through the hiatus in adductor magnus to enter the popliteal deep plantar arch which is completed by the termination of the space. From above, it descends on the posterior surface of the femur, dorsalis pedis artery. The arch gives rise to plantar metatarsal the capsule of the knee joint and then on the fascia overlying popliteus branches which supply the toes (Fig. In the fossa it is the deepest structure, ren- sends branches which join with the plantar metatarsal branches of dering it difficult to feel its pulsations. The popliteal vein crosses the the lateral plantar artery to supply the toes. The peroneal branch of the posterior tibial may arise Peripheral vascular disease (Fig. Atheroma causes narrowing of the peripheral arteries with a con- • Branches: muscular, sural and five genicular arteries are given off. Whilst flow may be adequate for tissue The last form a rich anastomosis around the knee. When symptoms are intolerable, pain is present at The anterior tibial artery rest or ischaemic ulceration has occurred, arterial reconstruction is • Course: the anterior tibial artery passes anteriorly from its origin, required. Reconstruction is performed using either the patient’s own accompanied by its venae comitantes, over the upper border of the inter- saphenous vein or a synthetic graft (Dacron or PTFE) to bypass the osseous membrane and then descends over the anterior surface of the occlusion. Disease which is limited in extent may be suitable for inter- membrane giving off muscular branches to the extensor compartment ventional procedures such as percutaneous transluminal angioplasty of the leg. The artery crosses the front of the ankle joint midway be- (PTA) or stent insertion. The arteries of the lower limb 95 43 The veins and lymphatics of the lower limb From lower abdomen Inguinal lymph nodes From perineum and gluteal region Vein linking great and small saphenous veins Great saphenous vein Popliteal lymph nodes Short saphenous vein Fig. The arrows indicate the direction of lymph flow Superficial epigastric Inguinal ligament Femoral Pubic tubercle artery Edge of saphenous opening Superficial Femoral vein circumflex Deep fascia of thigh iliac Superficial external pudendal Great saphenous vein Fig. Failure of this ‘muscle pump’ to work efficiently, towards becoming varicose and consequently often require surgery. It passes anterior to the medial malleolus, Varicose veins along the anteromedial aspect of the calf (with the saphenous nerve), These are classified as: migrates posteriorly to a handbreadth behind patella at the knee and • Primary: due to inherent valve dysfunction. It pierces the • Secondary: due to impedance of flow within the deep venous circula- cribriform fascia to drain into the femoral vein at the saphenous open- tion. These can occur in pregnancy or due to obstruction caused by ing. The terminal part of the great saphenous vein usually receives pelvic tumours or previous deep venous thrombosis. At surgery these help to distinguish the saphenous sure and become varicose. Anteromedial and posterolateral femoral (lateral The lymphatics of the lower limb (Fig. The superficial inguinal group lie in the superficial fascia and ous opening. They receive lymph from the majority of the superficial tis- below the medial malleolus, in the gaiter area, in the mid-calf region, sues of the lower limb. The valves • Horizontal chain: these lie parallel to the inguinal ligament. They in the perforators are directed inwards so that blood flows from receive lymph from the superficial tissues of the: lower trunk below the superficial to deep systems from where it can be pumped upwards level of the umbilicus, the buttock, the external genitalia and the lower assisted by the muscular contractions of the calf muscles. The superficial nodes drain into the deep nodes tem is consequently at higher pressure than the superficial and thus, through the saphenous opening in the deep fascia. In addition they • The small saphenous vein arises from the lateral end of the dorsal also receive lymph from the skin and superficial tissues of the heel and venous network on the foot. It passes behind the lateral malleolus and lateral aspect of the foot by way of the popliteal nodes. The deep nodes over the back of the calf to pierce the deep fascia in an inconstant posi- convey lymph to external iliac and thence to the para-aortic nodes. Obstruction of lymphatics results in lymphoedema (Fig. This can be congenital, due to aberrant lymphatic formation, or acquired The deep veins of the lower limb such as post radiotherapy or following certain infections. In develop- The deep veins of the calf are the venae comitantes of the anterior and ing countries infection with Filaria bancrofti is a significant cause of posterior tibial arteries which go on to become the popliteal and lymphoedema that can progress to massive proportions requiring limb femoral veins. The deep veins form an extensive network within the reduction or even amputation. The veins and lymphatics of the lower limb 97 44 The nerves of the lower limb I Anterior superior iliac spine Inguinal ligament Lateral cutaneous External oblique aponeurosis nerve of thigh Femoral nerve Femoral artery Iliacus Femoral vein Femoral canal Psoas tendon Lacunar ligament Pubic tubercle Lateral cutaneous nerve of thigh Pectineus Iliacus Inguinal ligament Femoral nerve Pubic tubercle Nerve to sartorius To pectineus Tensor fasciae latae Pectineus To vastus lateralis Adductor longus Psoas Femoral vein To vastus intermedius Great saphenous vein and rectus femoris Femoral artery Sartorius Saphenous nerve Intermediate To vastus medialis cutaneous nerve Medial cutaneous of thigh nerve of thigh (Skin of front of thigh) (Skin of medial thigh) Rectus femoris Gracilis Obturator externus Pectineus Posterior division Adductor Adductor brevis longus Anterior division Gracilis Deep fascia (Skin of medial leg Branch to and foot) Fig. The upper diagram shows the structures that pass under the inguinal ligament Fig. The latter supply • Course: the majority of the branches of the plexus pass through the sartorius and pectineus. The latter nerve is the only branch to extend • Intra-abdominal branchesathese are described in Chapter 21. It pierces the deep fascia overlying the adductor • Femoral nerve (L2,3,4)asee below. Obese patients sometimes describe paraesthesiae over the • Origins: the anterior divisions of the anterior primary rami of lateral thigh. This is termed meralgia paraesthetica and results from L2,3,4. It descends through the iliac fossa to pass under the inguinal compartment: ligament.