Reading the answers, the first thing that is clear to us is that acenocoumarol should NOT be given to a pregnant woman because of the risk of teratogenicity. Anyone who does so during residency should be punished with 100 slaps on the back. We discard answer 5. Second: if treatment is given, it should be during the entire pregnancy, prothrombotic status is not only during the puerperium, so answer 2 discarded. Advise a woman not to become pregnant when there are treatments that ensure a very low risk of thrombosis and/or fetal involvement? Answer 1 discarded. We are left with the possibility of not giving any treatment because it is low risk or administering low-dose aspirin. It is true that factor V Leiden in heterozygosis is classified as low risk, who has not presented a previous thrombotic episode nor is there a combination with another thrombophilia; if we look at the CHEST guide, VIII edition and review what was said at the last congress of the Spanish Society of Gynecology and Obstetrics, we see that aspirin is used in case of phospholipid syndrome and that in the case of this woman, without previous thrombosis, without previous abortions (at least two are needed) and also being heterozygous, treatment is not necessary. Correct answer, 3.

Reading the answers, the first thing that is clear to us is that acenocoumarol should NOT be given to a pregnant woman because of the risk of teratogenicity. Anyone who does so during residency should be punished with 100 slaps on the back. We discard answer 5. Second: if treatment is given, it should be during the entire pregnancy, prothrombotic status is not only during the puerperium, so answer 2 discarded. Advise a woman not to become pregnant when there are treatments that ensure a very low risk of thrombosis and/or fetal involvement? Answer 1 discarded. We are left with the possibility of not giving any treatment because it is low risk or administering low-dose aspirin. It is true that factor V Leiden in heterozygosis is classified as low risk, who has not presented a previous thrombotic episode nor is there a combination with another thrombophilia; if we look at the CHEST guide, VIII edition and review what was said at the last congress of the Spanish Society of Gynecology and Obstetrics, we see that aspirin is used in case of phospholipid syndrome and that in the case of this woman, without previous thrombosis, without previous abortions (at least two are needed) and also being heterozygous, treatment is not necessary. [HIDDEN].

A 25-year-old woman who wishes to become pregnant and wants to know what treatment she should take during the eventual pregnancy, as she is a heterozygous factor V Leiden carrier. She has never had any thrombotic phenomena. The determination of this factor was performed as a family study after an episode of pulmonary embolism in a sibling. What treatment should be advised?

Since pregnancy is a prothrombotic state, there would be a high risk of venous thromboembolism, so pregnancy should be discouraged.

Treatment with low molecular weight heparin at prophylactic doses should be carried out in the immediate puerperium, with optional follow-up during pregnancy.

Factor V Leiden in heterozygosis is a low-risk thrombophilia and there is no need for any treatment in pregnancy and puerperium.

Low-dose aspirin should be advised during pregnancy and puerperium.

Treatment with antivitamin K drugs (acenocoumarol) during pregnancy.

[Thrombophilia and pregnancy].

The risk of venous thromboembolism (VTE) increases up to 5-10-fold during pregnancy and VTE represents the first cause of maternal mortality. The annual incidence of VTE is 0.97 per 1000 women during pregnancy and 7.19 per 1000 in the puerperium. The risk is higher in carriers of inherited thrombophilia. Prophylaxis of VTE during pregnancy in thrombophilic women, is still controversial, whereas there is agreement on the used of LMWH or oral anticoagulants during puerperium. LMWH is suggested during pregnancy in antithrombin deficient women, compound heterozygotes for prothrombin G20210A and factor V Leiden, and homozygotes for these conditions, with no prior VTE. In heterozygotes for F V Leiden or prothrombin G20210A with no prior VTE surveillance is preferred during pregnancy and LMWH or OA during puerperium. For patients with APLAs and no prior VTE or fetal loss, one of the following approaches is suggested: prophylactic LMWH and/or low-dose aspirin, mini dose heparin, surveillance (7 degrees ACCP). Patients with APLAs and a history of thrombosis should receive therapeutic-dose LMWH or UH plus low-dose aspirin during pregnancy and long term OA postpartum. In women with prior VTE and inherited thrombophilia, prophylactic or intermediate-dose LMWH is recommended during pregnancy plus post-partum OA. Intermediate-dose LMWH during pregnancy is suggested in antithrombin-deficient women, compound heterozygotes for prothrombin G20210A and factor V Leiden, and homozygotes for these conditions.

Anticoagulation in pregnancy and the puerperium.

For the management of acute thrombotic events in pregnancy therapeutic doses of low molecular weight heparins (LMWH) may be used, unless the shorter half-life of intravenous unfractionated heparin (UH) and predictable reversibility by protamine are important. Treatment should be continued up until delivery and into the puerperium. Pregnant women who have had an acute thrombotic event should be delivered by a specialist team. In the case of recent thrombosis, delivery should be planned and the time during which anticoagulation therapy is ceased around the time of delivery should be minimised. Therapeutic doses of LMWH contraindicate the use of regional anaesthesia, and a switch to intravenous UH before delivery may allow greater flexibility in this regard. Prophylactic doses of LMWH can be used to reduce the risk of recurrent thromboembolic events in pregnancy. The regimen used will depend on the previous history, the family history and the presence of risk factors, including the genetic and acquired causes of thrombophilia. Women with mechanical heart valves are at high risk during pregnancy and require therapeutic anticoagulation throughout pregnancy under the direction of experienced specialists. Low-dose aspirin can reduce the risk of recurrent pre-eclampsia by about 15%, but the role of UH and LMWH in the prevention of recurrent miscarriage or obstetric complications associated with uteroplacental insufficiency is still uncertain.

Diagnosis, treatment, and prevention of venous thromboembolism in pregnancy.

Pregnancy and the puerperium put women at increased risk of venous thromboembolism (VTE) due to both baseline maternal risk factors and the development of pregnancy-related prothrombotic anatomic and physiologic changes. Pregnant women are at an approximately 5-fold increased risk of VTE compared with nonpregnant women, and the risk of VTE increases further (to ≥ 20-fold) in puerperium; risk remains increased until approximately 12 weeks postpartum. Pregnancy-related VTE accounts for about 10% of maternal deaths in the developed world. Clinicians should promptly evaluate any signs or symptoms suspicious for VTE, generally starting with ultrasound of the lower extremities. For treatment of women with established VTE, low molecular weight heparins (LMWHs) are preferred due to a favorable safety and efficacy profile. Unfractionated heparin (UFH) and potentially fondaparinux are alternatives. Warfarin should be avoided in the antepartum period due to teratogenicity, and the non-vitamin K oral anticoagulants are currently not recommended due to the lack of data. Low molecular weight heparin, UFH, and warfarin are all acceptable in the postpartum period and for breast-feeding women, but the non-vitamin K oral anticoagulants should be avoided. Prophylaxis (generally with LMWH or in some cases UFH) is recommended for women at highest risk of pregnancy-related VTE, such as those with inherited thrombophilias and a strong family or personal history of VTE. Prophylaxis with LMWH and aspirin is recommended for women with antiphospholipid syndrome. Clinicians should engage in multidisciplinary discussion, particularly around the time of delivery, to manage the details of anticoagulation in their pregnant patients.

Anticoagulation during pregnancy.

Venous thromboembolism (VTE) occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium. In the general population the incidence of pregnancy-associated VTE is approximately 1 in 1500 deliveries. The risk of VTE is five times higher in a pregnant than in a nonpregnant woman. Postpartum the VTE risk is even higher. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. Women with previous VTE have an approximately 3.5-fold increased risk of recurrent VTE during pregnancy. Heparin does not cross the placenta and is therefore the anticoagulant of choice. In case of acute thrombosis during pregnancy, treatment is performed in the same manner as for nonpregnant patients. There is an ongoing debate whether pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. Patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality, or a history of a severe thrombotic event (pulmonary embolism or extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Postpartum prophylaxis should be given to all women with an increased risk for VTE. A large body of evidence has been presented that hypercoagulability may cause recurrent abortions, stillbirth, and preeclampsia. There is no doubt that the antiphospholipid syndrome is strongly associated with fetal loss. The combination of heparin and aspirin significantly decreases the fetal loss rate during pregnancy and thus this is the treatment of choice in this patient group. Several studies indicate that women with recurrent miscarriage may benefit from heparin administration during pregnancy, however, data from controlled trials have not yet been published. In women with artificial heart valves, maternal and fetal complications are frequent despite anticoagulation, but oral anticoagulants can reduce the risk for maternal complications.

The risk of recurrent venous thromboembolism in pregnancy and puerperium without antithrombotic prophylaxis.

Whether or not pregnant women with a previous episode of venous thromboembolism (VTE) should receive antithrombotic prophylaxis is a matter of debate. In order to estimate the rate of recurrent deep venous thrombosis (DVT) or pulmonary embolism (PE) during pregnancy and puerperium we retrospectively investigated a cohort of 1104 women with previous VTE; after a single DVT or isolated PE, 88 of them became pregnant at least once without receiving antithrombotic prophylaxis. Overall, 155 pregnancies and 120 puerperium periods without prophylaxis were recorded. There were nine recurrences during pregnancy and 10 during puerperium, with a rate of 5.8% [95% confidence interval (CI) 3.0-10.6] and 8.3% (95%CI 4.5-14.6) respectively. In pregnancy, the rate of recurrence was 7.5% (95%CI 4.0-13.7) if the first VTE was unprovoked, related to pregnancy or to oral contraceptive use, whereas no recurrence occurred if the first VTE was related to other transient risk factors. In puerperium, the rate of recurrence was 15.5% (95%CI 7.7-28.7) in women with a pregnancy-related first VTE, with a risk 3.9-times higher than in the remaining women. Inherited thrombophilia was not associated with a statistically significant increase in risk of recurrence in pregnancy or in puerperium, yet the rate of recurrence in puerperium was 14.2% (95%CI 5.7-31.4) in overall carriers of factor V Leiden and 30% (95%CI 10.7-60.3) in carriers with a pregnancy-related first VTE, with a risk 6.8 times higher than in women without thrombophilia and with a non pregnancy-related first VTE.

Favorable outcome under anticoagulant therapy in a high risk pregnancy case report and short review of the (recent) literature.

The incidence of venous thromboembolism is significantly increased during pregnancy, recurrent venous thromboembolism being a serious complication because it is potentially life-threatening. According to recent ACCP guidelines, women with "high-risk" thrombophilias (e.g., homozygosity for factor V Leiden) who had a single prior episode of VTE treated with oral anticoagulants, should receive LMWH or UFH during pregnancy and puerperium, followed by resumption of long-term anticoagulants postpartum.We present the case of a young woman with a history of severe deep vein thrombosis of the inferior vena cava, occurring during oral contraceptive use. Subsequent investigation revealed homozygosity for Leiden mutation. She was treated with enoxaparin throughout gestation and 6 weeks postpartum and no complications appeared.

[Thrombophilia, preeclampsia and other pregnancy complications].

The aim of this paper is to present the latest developments in therapy and prophylaxis of deep vein thrombosis and other pregnancy complications in women with inherited or acquired thrombophilia and in women with mechanical heart valves. The data presented in the paper have been extracted from the Current Contents database. It is well known that the hypercoagulable state in pregnant women, caused either by the physiological changes of pregnancy or by inherited thrombophilia, increases the risk of venous thromboembolism (VTE), pulmonary embolism (PE), preeclampsia, recurrent early and late fetal loss, intrauterine growth retardation (IUGR), placental abruption, and other less probable complications of pregnancy and its outcome. In women with mechanical heart valves, the risk of systemic embolism is also seen to increase during pregnancy. According to data analyzed, positive antiphospholipid antibodies (APLA) as well as anticardiolipin antibody and lupus anticoagulant (nonspecific inhibitor) positivity, homozygosity and heterozygosity for factor V Leiden mutation and heterozygosity for the prothrombin G20210A variant, MTHFR C677T variant homozygosity and hyperhomocysteinemia are in strong association with pregnancy complications and severe pregnancy outcome. The strongest association for late fetal loss was seen in women with protein S deficiency. In order to reduce such risks, anticoagulation therapy is administered throughout pregnancy. The antithrombotic agents available for the prevention and treatment of VTE during pregnancy and pregnancy complications include unfractionated heparin (UFH), low-molecular-weight heparin (LMWH) and aspirin. Vitamin K antagonists are contraindicated in pregnancy. Low-dose aspirin may have a role in the prevention of some pregnancy complications, although its safety in early pregnancy is uncertain. LMWH and UFH are quite safe and efficacious when properly selected, dosed and monitored. The efficacy and safety of LMWH have been demonstrated in the prevention and treatment of VTE in pregnancy. LMWH in association with aspirin administered throughout pregnancy have been shown to be associated with a lower risk of complications in women with APLA syndrome. Women at a high risk of preeclampsia are recommended to use low-dose aspirin throughout pregnancy. When there is a history of preeclampsia, the administration of anticoagulation therapy is not recommended as a prophylaxis in subsequent pregnancies, as the risk appears to be already decreased as compared with previous pregnancy. LMWH has probable advantages over UFH for the incidence of side effects. In pregnant women with mechanical heart valves, anticoagulant therapy during pregnancy should include assessment of additional risk factors for thromboembolism including valve type, position, and history of thromboembolism, and decision should also be strongly influenced by the patient's preferences. If the risk of thromboembolism in patients with mechanical heart valves is considered very high, and efficacy or safety of prophylaxis with UFH or LMWH is not satisfactory (older-generation prosthesis in the mitral position or history of thromboembolism), administration of vitamin K antagonists throughout pregnancy is recommended with replacement by UFH or LMWH close to delivery. It should be considered that limited effectiveness of UFH or LMWH in patients with mechanical heart valves might be due to inadequate dosing. The necessity of anticoagulation therapy in women with inherited or acquired thrombophilia is biologically plausible; nevertheless, optimum management in such cases remains unknown.

Thrombosis during pregnancy: risk factors, diagnosis and treatment.

Venous thromboembolism occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium and remains a diagnostic and therapeutic challenge. In the general population the incidence of pregnancy associated VTE has been estimated to vary from 1 in 1000 to 1 in 2000 deliveries. The risk of VTE is five times higher in a pregnant woman than in a nonpregnant woman of similar age. Postpartum VTE is more common than antepartum VTE. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose deep-vein thrombosis clinically is generally poor and is further hampered during pregnancy since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury. Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant treatment of choice during pregnancy. In case of acute new onset of thrombosis during pregnancy, treatment is performed like in non-pregnant patients with acute deep vein thrombosis or pulmonary embolism. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.

Venous thromboembolism, thrombophilia, antithrombotic therapy, and pregnancy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition).

This article discusses the management of venous thromboembolism (VTE) and thrombophilia, as well as the use of antithrombotic agents, during pregnancy and is part of the American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Grade 1 recommendations are strong and indicate that benefits do, or do not, outweigh risks, burden, and costs. Grade 2 recommendations are weaker and imply that the magnitude of the benefits and risks, burden, and costs are less certain. Support for recommendations may come from high-quality, moderate-quality or low-quality studies; labeled, respectively, A, B, and C. Among the key recommendations in this chapter are the following: for pregnant women, in general, we recommend that vitamin K antagonists should be substituted with unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) [Grade 1A], except perhaps in women with mechanical heart valves. For pregnant patients, we suggest LMWH over UFH for the prevention and treatment of VTE (Grade 2C). For pregnant women with acute VTE, we recommend that subcutaneous LMWH or UFH should be continued throughout pregnancy (Grade 1B) and suggest that anticoagulants should be continued for at least 6 weeks postpartum (for a total minimum duration of therapy of 6 months) [Grade 2C]. For pregnant patients with a single prior episode of VTE associated with a transient risk factor that is no longer present and no thrombophilia, we recommend clinical surveillance antepartum and anticoagulant prophylaxis postpartum (Grade 1C). For other pregnant women with a history of a single prior episode of VTE who are not receiving long-term anticoagulant therapy, we recommend one of the following, rather than routine care or full-dose anticoagulation: antepartum prophylactic LMWH/UFH or intermediate-dose LMWH/UFH or clinical surveillance throughout pregnancy plus postpartum anticoagulants (Grade 1C). For such patients with a higher risk thrombophilia, in addition to postpartum prophylaxis, we suggest antepartum prophylactic or intermediate-dose LMWH or prophylactic or intermediate-dose UFH, rather than clinical surveillance (Grade 2C). We suggest that pregnant women with multiple episodes of VTE who are not receiving long-term anticoagulants receive antepartum prophylactic, intermediate-dose, or adjusted-dose LMWH or intermediate or adjusted-dose UFH, followed by postpartum anticoagulants (Grade 2C). For those pregnant women with prior VTE who are receiving long-term anticoagulants, we recommend LMWH or UFH throughout pregnancy (either adjusted-dose LMWH or UFH, 75% of adjusted-dose LMWH, or intermediate-dose LMWH) followed by resumption of long-term anticoagulants postpartum (Grade 1C). We suggest both antepartum and postpartum prophylaxis for pregnant women with no prior history of VTE but antithrombin deficiency (Grade 2C). For all other pregnant women with thrombophilia but no prior VTE, we suggest antepartum clinical surveillance or prophylactic LMWH or UFH, plus postpartum anticoagulants, rather than routine care (Grade 2C). For women with recurrent early pregnancy loss or unexplained late pregnancy loss, we recommend screening for antiphospholipid antibodies (APLAs) [Grade 1A]. For women with these pregnancy complications who test positive for APLAs and have no history of venous or arterial thrombosis, we recommend antepartum administration of prophylactic or intermediate-dose UFH or prophylactic LMWH combined with aspirin (Grade 1B). We recommend that the decision about anticoagulant management during pregnancy for pregnant women with mechanical heart valves include an assessment of additional risk factors for thromboembolism including valve type, position, and history of thromboembolism (Grade 1C). While patient values and preferences are important for all decisions regarding antithrombotic therapy in pregnancy, this is particularly so for women with mechanical heart valves. For these women, we recommend either adjusted-dose bid LMWH throughout pregnancy (Grade 1C), adjusted-dose UFH throughout pregnancy (Grade 1C), or one of these two regimens until the thirteenth week with warfarin substitution until close to delivery before restarting LMWH or UFH) [Grade 1C]. However, if a pregnant woman with a mechanical heart valve is judged to be at very high risk of thromboembolism and there are concerns about the efficacy and safety of LMWH or UFH as dosed above, we suggest vitamin K antagonists throughout pregnancy with replacement by UFH or LMWH close to delivery, after a thorough discussion of the potential risks and benefits of this approach (Grade 2C).

[Current management of thromboembolism in pregnancy and puerperium].

Venous thromboembolism (VTE) remains the leading cause of maternal death. Today, various risk factors and conditions are known to increase the risk for VTE associated with pregnancy. Having identified the individual risk of a pregnant women, appropriate preventive measures can be taken. If VTE occurs during pregnancy, an appropriate immediate diagnostic work-up is essential in order to avoid further complications. For deep vein thrombosis (DVT) the diagnostic tool of choice is color-coded duplex-sonography, for pulmonary embolism (PE) perfusion/ventilation lung scan can be used. Integrating a detailed individual and family history, the presence of thrombophilia or other risk factors, a risk stratification can be undertaken. These risk categories are defined in the present paper and the appropriate treatment measures are described. As oral anticoagulants cross the placenta and may cause embryopathy in any trimester, oral anticoagulants should be avoided throughout pregnancy. Therefore, heparin is the anti-coagulant of choice for pregnant women, with low molecular weight heparins (LMWH) having distinctive pharmacological advantages over unfractionated heparins. Besides a potential for bleeding, the main side effects of heparin include heparin-induced thrombocytopenia which prompts for platelet monitoring, especially in the first weeks of heparin treatment, and, secondly, heparin-induced osteoporosis, which is a potential sequel of long-term heparin administration. Even though there are abundant reports in the literature on the use of LMWH in pregnant women, that show that they are safe and effective, LMWH are not specifically licensed for the use in pregnancy.

Pregnancy-associated thrombosis.

Venous thromboembolism (VTE) occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium. In the general population the incidence of pregnancy associated VTE is approximately 1 in 1500 deliveries The risk of VTE is five times higher in a pregnant than in a non-pregnant woman. Postpartum the VTE-risk is even higher. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose pregnancy-associated VTE clinically is generally poor, since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant of choice. In case of acute thrombosis during pregnancy, treatment is performed like in nonpregnant patients. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.

Thrombophilia and anticoagulation in pregnancy: indications, risks and management.

Venous thromboembolism (VTE) is a leading cause of maternal morbidity and mortality in pregnancy and the puerperium. To reduce the incidence of VTE, it is helpful to understand the haemostatic changes during pregnancy and to recognise thrombophilic states. According to the individual risk profile a prophylactic or therapeutic anticoagulation needs to be considered. A narrative, non-systematic overview of articles published in English, German or French over the past three decades with an emphasis on manuscripts from 2003 to 2008. Heparins are the main agents used for anticoagulation during pregnancy. Low-molecular-weight heparins have more advantages than unfractionated heparin and should be preferred. Vitamin-K antagonists are not recommended in this condition as first-line treatment because of the risk for embryopathy and fetal bleeding, but they can be given under certain conditions. Subgroups of patients, such as women with prosthetic heart valves, require special attention. Adverse pregnancy outcomes due to hereditary thrombophilia are new indications for use of anticoagulants during pregnancy. National and international guidelines on prevention and treatment of thromboembolism are helpful in applying the proper regimen in pregnant women.

[VENOUS THROMBOEMBOLISM DURING PREGNANCY AND THE PUERPERIUM - WHO? WHEN? AND HOW TO TREAT?]

Venous thromboembolism (VTE) is a potentially life-threatening medical condition during pregnancy and the puerperium. During pregnancy, the risk of VTE is increased four to tenfold compared to non-pregnant women of comparable age. The risk is even higher in the puerperium. Physician awareness followed by adequate treatment may reduce the number of events. The most important risk factors are previous VTE or thrombophilia, although other acquired risk factors may result in similar impacts. Treatment is based on personalized risk assessment at the first patient visit during pregnancy, followed by repeated assessment of complications or at admission and final assessment at delivery. Hydration and mobilization are advised for all women. Pharmacological prevention by low-molecular-weight heparin (LMWH) is advised based on risk stratification. International guidelines differ by indications and range of management options. The purpose of this review is to summarize our knowledge on risk factors for VTE during pregnancy and puerperium and guide management options.

[The frequency of venous thromboembolism in women with Leiden mutation in association with pregnancy and puerperium].

The assessment of the frequency of venous thromboembolism (VTE) in women with F V Leiden in association with pregnancy and puerperium and according these results and available data to formulate the principles of thromboprophylaxis. Retrospective case control study. The assessment of frequency of VTE in the group of 224 women with F V Leiden in heterozygous form in association with 460 pregnancies and in the group of 40 women with F V Leiden in homozygous form in association with 70 pregnancies. This frequency of VTE in those groups was compared with the frequency of VTE in the control group of 201 women without F V Leiden in association with 422 pregnancies. F V Leiden evaluation was done in the period of 1996-2003. In the group of women with F V Leiden in heterozygous form VTE occurred 44-fold during pregnancy and puerperium. In 17 cases VTE was manifested in pregnancy (once in Ist trimester, twice in IInd trimester, 14 times in IIIrd trimester), in 27 women VTE occurred in puerperium and always within the first 10 days after delivery. Proximal venous thrombosis was diagnosed in 34 cases, in 5 cases being complicated by pulmonary embolism. In 10 women thrombosis was distal. The frequency of VTE is 9.6%. In the group of women with homozyous form VTE occurred in 14 cases (20%). In 5 cases VTE occurred during pregnancy, in 9 cases after delivery and in all cases within first 2 weeks after delivery. The frequency of VTE in the control group is 0.24%. The results were statistically assessed by Fishers exact test in programme NCSS 2004. Frequency of VTE in both cohorts of women with F V Leiden reached statistical significance in comparison with the control group. Pregnancy and puerperium are significant risk factors for VTE in the group of women with F V Leiden in heterozygous form and mainly in homozygous form.

The management of thrombosis in pregnancy: role of low-molecular-weight heparin.

Fatal pulmonary embolism remains the most common cause of mortality among pregnant women in many Western countries. The physiological changes of pregnancy produce a hypercoagulable state that increases the risk of venous thromboembolism (VTE). Women with inherited or acquired thrombophilias are at particularly high risk of VTE during pregnancy, and thromboprophylaxis may be advisable in some cases. Thrombophilia is also associated with complications of pregnancy, including fetal loss, pre-eclampsia, intra-uterine growth restriction, and placental abruption. The antithrombotic agents available for the prevention and treatment of VTE during pregnancy, and pregnancy complications, include unfractionated heparin (UFH), low-molecular-weight heparin (LMWH) and aspirin. Vitamin K antagonists are contra-indicated in pregnancy. Low-dose aspirin may have a role in the prevention of some pregnancy complications, although its safety in early and late pregnancy is uncertain. The efficacy and safety of LMWHs have been demonstrated for the prevention and treatment of VTE in pregnancy. These agents are increasingly being used in place of UFH, which is associated with a higher incidence of side effects compared with LMWH, in addition to the need for regular laboratory monitoring. Evidence is also emerging to support the use of LMWH in the prevention of recurrent fetal loss, although further trials are needed to explore the role of LMWHs in this indication and in the prevention of other complications of pregnancy.

Efficacy and safety of nadroparin and unfractionated heparin for the treatment of venous thromboembolism during pregnancy and puerperium.

The optimal treatment of pregnancy associated VTE (venous thromboembolism) has not been established yet. The assessment of the efficacy and safety of low molecular weight heparin (LMWH) nadroparin and unfractionated heparin (UFH) used for the treatment of pregnancy and puerperium related VTE. Primary study goals were to analyze the incidence of recurrent VTE (proximal extension or pulmonary thromboembolism), thrombocytopenia, major and minor hemorrhages and skin allergic reactions. The study also included the incidence of miscarriages, stillbirth and neonatal abnormalities. We also studied the relationship between the presence of thrombophilia and the occurrence of complications during VTE treatment. Seventy-two women with antepartal VTE treated with s.c. LMWH during entire pregnancy and 88 women with postpartal VTE initially treated with either s.c. LMWH or i.v.UFH were under follow-up during the entire treatment. Thrombophilia testing included antithrombin, protein C and protein S activity levels, Activated protein C (APC) resistance, LA, ACL, FV Leiden, FII G20210A and MTHFR C677T mutations. Twice a day weight based therapeutic regimen was applied for LMWH and activated partial thromboplastin time (aPTT) adjusted UFH dosages. After 2-6 weeks of antepartal deep vein thrombosis (DVT) treatment the dose of nadroparin was reduced to intermediate level. The duration of LMWH therapy during pregnancy was 1-35 weeks, on average 16 weeks. One case (0.62%) of DVT propagation into the vena cava occurred in a woman with antithrombin deficiency treated with LMWH. Two women (1.25%) had minor bleeding and 5 (3.125%) had minimal bleeding, while 3 (1.9%) had skin allergic reactions. The rate of successful pregnancy outcome was 97.2%. There were no cases of stillbirth or neonatal congenital abnormalities. Thrombophilia was found in 86 women (53.7%). No statistically significant correlation between the presence of thrombophilia and treatment complications were found. Nadroparin is both safe and effective for the treatment of DVT during pregnancy and puerperium.

Pregnancy-Related Venous Thromboembolism.

Pregnancy is associated with an increased risk of venous thromboembolism (VTE), with a reported incidence ranging from 0.49 to 2 events per 1000 deliveries. Risk factors include advanced maternal age, obesity, smoking, and cesarian section. Women with a history of previous VTE are at a 4-fold higher risk of recurrent thromboembolic events during subsequent pregnancies. Additionally, the presence of concomitant thrombophilia, particularly factor V Leiden (homozygosity), prothrombin gene mutation (homozygosity), or antiphospholipid syndrome (APS), increases the risk of pregnancy-related VTE. Low-molecular-weight heparin (LMWH) and unfractionated heparin (UFH) are the drugs of choice for anticoagulation during pregnancy. LMWH is preferred due to ease of use and lower rates of adverse events. Women with high thromboembolic risk particularly those with a family history of VTE should receive antepartum thromboprophylaxis. Women with low thromboembolic risk or previous VTE caused by a transient risk factor (ie, provoked), who have no family history of VTE, may undergo antepartum surveillance. Postpartum anticoagulation can be considered in women with both high and low thromboembolic risk.

[Pregnancy-associated venous thromboembolic disease: prediction, prevention, and therapy].

Thromboembolic disease remains a leading cause of maternal mortality during pregnancy and the puerperium. Rational and risk-adapted administration of heparin prophylaxis depends on 1. the identification of those women who have an increased risk of thrombosis and 2. the accurate quantification of this risk. In women without prior thrombosis, the presence of a heterozygous factor V Leiden or heterozygous G20210A mutation in the prothrombin gene is associated with a pregnancy-associated thrombotic risk of approximately 1 in 400. Thus, in pregnant carriers of either one of these mutations the risk of venous thromboembolism is low. Therefore, no heparin prophylaxis is recommended. A combination of the two genetic risk factors can increase the risk to a modest level of 1 in 25. In women with a single episode of prior thrombosis associated with a transient risk factor, e.g. surgery or trauma, and no additional genetic risk factor, the probability of a pregnancy-associated thrombosis appears also to be low. However, data are sparse and conflicting. In contrast, in women with a prior idiopathic venous thrombosis who carry an additional hereditary risk factor or who have a positive family history of thrombosis, a high risk (>10%) can be expected supporting the indication for active antepartum and postpartum heparin prophylaxis. Despite the remarkable progress in risk stratification, the absolute magnitude of risk and the optimal management in many cases is an issue of ongoing debate.

Hypercoagulability in pregnancy

Strategies A consensus on the correct anticoagulation regimen during pregnancy is lacking. Treatment is tailored to the particular individual based on her risk of complications. Warfarin and other vitamin K-inhibiting agents are contraindicated during the first trimester of pregnancy because of the teratogenic effects, and should not be administered when the pregnancy is confirmed. Rather, women who are on chronic anticoagulation may be given the option of conversion to either unfractionated heparin or low molecular weight heparin (LMWH), such as tinzaparin, prior to a planned conception. LMWH is as safe and efficacious as unfractionated heparin. A blood test including platelets and a clotting screen should be performed prior to administration of anticoagulant regimens in pregnancy.

Prophylaxis and Therapy of Venous Thrombotic Events (VTE) in Pregnancy and the Postpartum Period.

Venous thromboembolisms and pulmonary embolisms are one of the main causes of morbidity and mortality in pregnancy. The increased risk of thrombotic events caused by the physiological changes during pregnancy alone does not justify any medical antithrombotic prophylaxis. However, if there are also other risk factors such as a history of thromboses, hormonal stimulation as part of fertility treatment, thrombophilia, increased age of the pregnant woman, severe obesity or predisposing concomitant illnesses, the risk of thrombosis should be re-evaluated - if possible by a coagulation specialist - and drug prophylaxis should be initiated, where applicable. Low-molecular-weight heparins (LMWH) are the standard medication for the prophylaxis and treatment of thrombotic events in pregnancy and the postpartum period. Medical thrombosis prophylaxis started during pregnancy is generally continued for about six weeks following delivery due to the risk of thrombosis which peaks during the postpartum period. The same applies to therapeutic anticoagulation after the occurrence of a thrombotic event in pregnancy; here, a minimum duration of the therapy of three months should also be adhered to. During breastfeeding, LMWH or the oral anticoagulant warfarin can be considered; neither active substance passes into breast milk.

Evidence-based indications for thrombophilia screening.

Thrombophilic defects have been shown to be associated with an increased risk of venous thrombosis, fetal loss, and gestational complications. The knowledge about the clinical relevance of thrombophilic defects is increasing, and evidence-based indications for thrombophilia screening are therefore discussed in this review. Selective thrombophilia screening based on previous personal and/or family history of venous thromboembolism is more cost-effective than universal screening in all patient groups evaluated. In the majority of patients with acute venous thrombosis, the results of thrombophilia screening do not influence the duration of oral anticoagulation. The only patient population who clearly profits from thrombophilia screening in this situation are patients with a newly diagnosed antiphospholipid syndrome, because prolonged anticoagulation can avoid the high incidence of recurrence in this patient population. Because of the increased risk of venous thrombosis during pregnancy and the puerperium, thrombophilia screening is indicated in selected patients with a previous history of venous thrombosis or a positive family history. Significant associations with early and late pregnancy loss are observed for carriers of the heterozygous factor V Leiden mutation, the heterozygous prothrombin-mutation G20210A and anticardiolipin antibodies, while protein S deficiency is significantly associated with late pregnancy loss. Antithrombotic drugs like UFH, LMWH or low-dose aspirin may have a potential therapeutic benefit in patients with recurrent pregnancy loss and thrombophilia, but placebo-controlled, multicenter trials are urgently needed to clarify this issue. Although a supra-additive effect for the risk of venous thrombosis is observed between oral contraceptives and some thrombophilias, the absolute incidence of venous thromboembolism is low in premenopausal women and mass screening strategies are therefore unlikely to be effective. While antiphospholipid antibodies are known to be associated with arterial thrombosis, screening for heritable thrombophilias is not useful in arterial thrombosis, although subgroup analysis indicates that they may play a role particularly in young patients and children.

Venous thromboembolism in pregnancy: diagnosis, management and prevention.

A pregnant woman has a two- to five-fold higher risk of venous thromboembolism (VTE) than a non-pregnant woman of the same age and, in developed countries, she is more likely to die from fatal pulmonary embolism (PE) than from obstetric haemorrhage. The increased VTE risk is mediated through normal physiological changes of pregnancy including alterations in haemostasis that favour coagulation, reduced fibrinolysis and pooling and stasis of blood in the lower limbs. Thrombophilia, smoking, obesity, immobility and postpartum factors such as infection, bleeding and emergency surgery (including emergency caesarian section) also increase the risk of pregnancy-related VTE. The diagnosis of VTE can be safely established with acceptable radiation exposure to the fetus using readily available imaging modalities such as ultrasound, ventilation perfusion lung scanning and computed tomographic pulmonary angiography. However, the optimal diagnostic strategies still remain to be determined. If there is no contraindication to anticoagulation, commencing treatment prior to objective confirmation should be strongly considered. For the mother and fetus, effective and safe treatment is readily available with low-molecular-weight heparin (LMWH), but optimal dosing of these agents in pregnancy remains controversial. Emerging data support antepartum LMWH prophylaxis for women with previous VTE if the event was unprovoked or in the presence of thrombophilia. On the other hand, women with prior provoked VTE and no thrombophilia or women with asymptomatic thrombophilia (but a family history of VTE) can safely be managed with antepartum surveillance. Postpartum prophylaxis is recommended for women with prior VTE or thrombophilia (and a family history of VTE).

Management of thromboembolic disease in pregnancy.

Venous thromboembolism (VTE) is the leading cause of maternal mortality and morbidity in developed countries including Singapore. The physiological changes of pregnancy and other factors, such as maternal age, parity, obesity, operative delivery, general anaesthesia and congenital and acquired thrombophilia, further increase the risk of VTE throughout all three trimesters of pregnancy, including the puerperium. VTE has a wide spectrum of clinical presentations and a high index of clinical suspicion is vital. Clinicians should not withhold the use of chest X-rays and ventilation-perfusion (V/Q) lung scans in pregnancy as the radiation emitted is well within the safety limits to the fetus. Most treatment guidelines are based on studies in non-pregnant populations. Heparin is the preferred anticoagulant as it does not cross the placenta and therefore carries no teratogenic risk to the fetus. There is increasing experience and confidence in the use of fixed dose subcutaneous low molecular weight heparin (LMWH) which removes the need for cumbersome monitoring, thereby allowing outpatient treatment. LMWH may also have a lower risk of osteopaenic complications compared to unfractionated heparin. With the exception of acute phase treatment of pulmonary embolism, LMWH is used in all other aspects of the treatment of VTE in pregnancy, including thromboprophylaxis. Risk stratification of women into high and low risk allows judicious use of anticoagulants for thromboprophylaxis. Antenatal thromboprophylaxis with LMWH is reserved for high-risk women, while low-risk women will only require such cover in the postpartum period.

Management of thromboembolism in pregnancy.

The incidence of venous thromboembolism is increased during pregnancy and the postpartum period. This risk is high for women with documented hereditary or acquired risk factors who have experienced a prior thrombotic event. These individuals require a minimum of prophylactic dose anticoagulation with unfractionated or low molecular weight heparin during pregnancy, with anticoagulation continuing for 4 to 6 weeks postpartum. Women receiving therapeutic dose anticoagulation with warfarin before pregnancy for a hereditary or acquired condition should be transitioned to therapeutic doses of unfractionated heparin or low molecular weight heparin before or within 6 weeks of becoming pregnant, and can then resume warfarin postpartum. Women experiencing a thromboembolic event during pregnancy should receive therapeutic treatment with unfractionated heparin or low molecular weight heparin during pregnancy, with anticoagulation continuing for 4 to 6 weeks postpartum, and for a total of at least 6 months.

[Prevention and treatment of thrombosis in pregnancy].

Pregnancy and especially delivery and the puerperium are associated with an increased risk of thromboembolic disease. Intravenous high dose heparin is the therapy of choice for manifest thromboembolic disease in pregnancy. However, high-dose heparin fails to prevent postthrombotic chronic venous insufficiency in more than one-third of the cases. Low-dose heparin may be used for antithrombotic prophylaxis during pregnancy. However, low-dose heparin may induce a substantial loss of bone density in up to 30% of cases and may be complicated by heparin-associated thrombopenia in up to 2%. This review discusses strategies to reduce these considerable risks. Prospective studies suggest that the risk of recurrence after prior deep vein thrombosis may be somewhat overestimated. These data suggest new therapeutic options in women with no risk factors other than a personal history of thrombosis. Improved diagnostic techniques may contribute to a better evaluation of the individual risk by assessing possible underlying problems such as resistance to activated protein C or deficiencies of coagulation inhibitors. Also, duration of prophylactic anticoagulation may be reduced by targeting treatment to periods of increased risk such as immobilisation, dehydration, surgery, delivery and the puerperium. Recently, evidence has been provided indicating that the use of low molecular weight heparins may be associated with reduced loss of bone density and a significantly attenuated risk of heparin-associated thrombopenia.

[Thromboprophylaxis during pregnancy and the puerperium: highlights from current guidelines].

Venous thromboembolism (VTE) is one of the leading causes of maternal deaths worldwide. Mortality and morbidity of VTE are potentially preventable, since two-thirds of these women have identifiable risk factors and may benefit from appropriate thromboprophylaxis. Individual and careful assessment of the personal and family history as well as the assessment of pre-existing and new-onset/transient risk factors during pregnancy and after delivery are mandatory for an effective prevention of VTE. Current guidelines (American College of Chest Physicians 2008, AWMF-Guideline 003/001 2009 and the Royal College Guideline No. 37 2009) provide practical recommendations for risk stratification regarding low, intermediate and high risk conditions. At high risk are women with previous VTE or thrombophilia. Corresponding to risk stratification grade C recommendations have been made for VTE prophylaxis during pregnancy and the puerperium. Prophylaxis with low molecular weight heparin (LMWH) should begin as early in pregnancy as practical. In women with lower risk mobilisation, avoidance of dehydration and mechanical methods (e. g., graduated compressive stockings) are sufficient. After delivery women with intermediate risk should be given LMWH for 7 days, women at high risk for 6 weeks or as long as additional risk factors are present. All women who have additional risk factors and who have had an elective Caesarean section should receive prophylactic LMWH for 7 days as should also all women who have had a Caesarean section in labour or an emergency Caesarean section. At the onset of labour, in case of any vaginal bleeding, prior to induction of labour or 12 h before an elective Caesarean section, antenatal LMWH prophylaxis should be discontinued, LMWH prophylaxis can be continued for 4-6 h after vaginal and for 6-12 h after Caesarean delivery when the women do not have an increased risk of haemorrhage. Current guidelines recommend than LMWH are the agents of choice for antenatal thromboprophylaxis; in comparison to unfractionated heparin, LMWH are associated with a substantially lower risk of heparin-induced thrombocytopenia and osteoporosis. Both oral anticoagulants and heparin are safe when breast-feeding.

[Indications and monitoring of antithrombotic prophylaxis for venous thromboembolism during pregnancy and post-partum].

Pregnancy and puerperium are well-known risk factors for venous thromboembolism, but the actual incidence of the disease is low (about 1/1,500 pregnancies). Pregnancy-associated venous thromboembolism is rare, though it is still the second cause of maternal death in France. Several types of prophylaxis are available, mainly clinical vigilance and aggressive investigation of women with symptoms of venous thromboembolism, or antithrombotic prophylaxis. Given the low incidence of the pathology, it seems desirable to select high-risk groups of women for such strategies. The most studied and identified risk factors are prior episodes of venous thromboembolism and biological thrombophilias. Prophylaxis through low molecular weight heparin during pregnancy and the puerperium should be considered mainly in these two groups. Noteworthy, no prospective and randomized study is available, and treatment recommendations are grade C.

Inherited thrombophilias and anticoagulation in pregnancy.

Thromboprophylaxis, primary or secondary, should be considered in selected pregnant women with inherited thrombophilias; such women may be divided into high-, medium- and low-risk categories on the basis of the specific thrombophilic defect and any personal or family history of venous thromboembolism (VTE). Women at high risk of VTE should receive treatment doses of low-molecular-weight heparin (LMWH) throughout pregnancy and should remain on anticoagulation for 6 weeks postpartum, or, where appropriate, long-term. Women at moderate risk should be treated with prophylactic fixed-dose LMWH throughout pregnancy and for 6 weeks postpartum. Women at low risk should receive prophylactic fixed-dose LMWH for 6 weeks postpartum, and low-dose aspirin LDA should be considered during pregnancy. LWMH offers important advantages over unfractionated heparin (UFH); heparin-induced thrombocytopaenia (HIT) and osteopaenia are rarely seen. For treatment doses of LMWH, dosage adjustment based on anti-Xa levels is usually required as pregnancy progresses. Warfarin should be avoided throughout pregnancy. LMWH, UFH and warfarin are safe for breast-feeding mothers.

Factor V Leiden

Women with factor V Leiden have a substantially increased risk of clotting in pregnancy (and on estrogen-containing birth control pills or hormone replacement) in the form of deep vein thrombosis and pulmonary embolism. They also may have a small increased risk of preeclampsia, may have a small increased risk of low birth weight babies, may have a small increased risk of miscarriage and stillbirth due to either clotting in the placenta, umbilical cord, or the fetus (fetal clotting may depend on whether the baby has inherited the gene) or influences the clotting system may have on placental development. Note that many of these women go through one or more pregnancies with no difficulties, while others may repeatedly have pregnancy complications, and still others may develop clots within weeks of becoming pregnant. See also Prothrombin G20210A References Further reading Factor V Leiden Thrombophilia Explained - Genome.gov External links

Obstetric complications and pregnancy-related venous thromboembolism: the effect of low-molecular-weight heparin on their prevention in carriers of factor V Leiden or prothrombin G20210A mutation.

Whether the administration of low-molecular-weight heparin (LMWH) during pregnancy is effective in preventing obstetric complications and pregnancy-related venous thromboembolism (VTE) in women who are carriers of factor V Leiden (FVL) and/or prothrombin variant G20210A (PTm) is controversial. This observational study investigated the possible efficacy of pharmacological treatment with LMWH ± aspirin (ASA) in pregnancy outcomes in 1,011 pregnancies of 416 women with thrombophilia (FVL and/or PTm). Most patients were chosen on the basis of previous obstetrical complications (36%), or because of familial or personal history of venous/arterial thromboembolism (28% and 18%, respectively); 74 patients (18%) were incidentally identified. The outcome was evaluated according to the type of treatment and of the period of pregnancy when the treatment was started. After adjustment for observation before and after diagnosis of thrombophilia, previous miscarriages and VTE, parity, age and centre, we observed that LMWH had a protective effect on miscarriages (odds ratio [OR] 0.52, 95% confidence interval [CI] 0.29-0.94) and VTE (OR 0.05, 95% CI 0.01-0.21). ASA appeared to have no effect on the prevention of obstetric complications and VTE. A nested analysis performed in 116 women with two or more obstetric complications confirmed that the highest number of live births was recorded in the group under LMWH prophylaxis (OR 0.19, 95% CI 0.05-0.75). These results suggest that LMWH prophylaxis reduces the risk of obstetric complications in carriers of FVL and/or PTm, particularly in those with previous obstetric events. Furthermore, LMWH prophylaxis reduces the risk of pregnancy-related VTE.

Hypercoagulability in pregnancy

A risk score of four points or higher means prophylaxis in the ante partum period is needed, as well as at least six weeks post partum. A previous distal DVT indicates a minimum of 12 weeks (three months) of therapeutic anticoagulation therapy. A previous proximal DVT or pulmonary embolism requires a minimum of 26 weeks (6.5 months) of therapy If the therapy duration reaches delivery time, the remaining duration may be given after delivery, possibly extending the minimum of six weeks of post partum therapy. In a very high risk, high-dose ante partum prophylaxis should be continued at least 12 weeks after delivery. Women with antiphospholipid syndrome should have an additional low-dose prophylactic treatment of aspirin. Cautions All anticoagulants (including LMWH) should be used with caution in women with suspected coagulopathy, thrombocytopaenia, liver disease and nephropathy.

Thrombophilia and pregnancy complications.

Venous thromboembolism is the leading cause of pregnancy-associated morbidity and mortality. Women with thrombophilia have an increased risk of VTE in pregnancy and puerperium. In individuals with hereditary thrombosis risk factors a relative risk of pregnancy associated VTE ranging from 3.4 to 15.2 has been found. Women with previous VTE have an approximately 3.5-fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Data on the association of thrombophilia and pregnancy loss and pre-eclampsia are conflicting. Besides an established association with antiphospholipid antibodies, available data suggest associations for antithrombin deficiency, hyper-homo-cysteinemia, factor V Leiden, prothrombin G20210A variation and protein S-deficiency. A contribution of thrombophilia to the risk of pre-eclampsia is less well established. A limited number of prospective studies did not reveal an increased risk of pregnancy complications in unselected women with thrombosis risk factors. Data of only one controlled trial on the prevention of pregnancy loss with low molecular weight heparin (LMWH) are available, which revealed a strikingly positive effect. Thrombophilia screening might be justified in women with pregnancy loss and treatment with LMWH might be considered in those with pregnancy loss and thrombophilia. Further prospective studies and controlled interventional trials are urgently needed.


We are being shown a picture of lumbar canal stenosis (Answer 4 correct). The patient shows the characteristic clinical picture: lumbar pain that is relieved by flexing the trunk forward, radicular pain with lower limb involvement and neurogenic claudication. Low back pain in a patient over 60 years of age accompanied by leg weakness when walking, which has to be interrupted at a certain distance, called neurogenic claudication, is the typical picture of stenosis. The patient is relieved by flexing the spine forward because it widens the lumbar canal and worsens with extension...

We are being shown a picture of lumbar canal stenosis ([HIDDEN]). The patient shows the characteristic clinical picture: lumbar pain that is relieved by flexing the trunk forward, radicular pain with lower limb involvement and neurogenic claudication. Low back pain in a patient over 60 years of age accompanied by leg weakness when walking, which has to be interrupted at a certain distance, called neurogenic claudication, is the typical picture of stenosis. The patient is relieved by flexing the spine forward because it widens the lumbar canal and worsens with extension...

The most likely diagnosis of a 74-year-old patient who since two months ago begins with lumbar pain radiating to lower limbs, neurogenic claudication and limitation to extension the trunk is:

Successful operative management of an upper lumbar spinal canal stenosis resulting in multilevel lower nerve root radiculopathy.

Lumbar stenosis is a common disorder, usually characterized clinically by neurogenic claudication with or without lumbar/sacral radiculopathy corresponding to the level of stenosis. We present a case of lumbar stenosis manifesting as a multilevel radiculopathy inferior to the nerve roots at the level of the stenosis. A 55-year-old gentleman presented with bilateral lower extremity pain with neurogenic claudication in an L5/S1 distribution (posterior thigh, calf, into the foot) concomitant with dorsiflexion and plantarflexion weakness. Imaging revealed grade I spondylolisthesis of L3 on L4 with severe spinal canal stenosis at L3-L4, mild left L4-L5 disc herniation, no stenosis at L5-S1, and no instability. EMG revealed active and chronic L5 and S1 radiculopathy. The patient underwent bilateral L3-L4 hemilaminotomy with left L4-L5 microdiscectomy for treatment of his L3-L4 stenosis. Postoperatively, he exhibited significant improvement in dorsiflexion and plantarflexion. The L5-S1 level was not involved in the operative decompression. Patients with radiculopathy and normal imaging at the level corresponding to the radiculopathy should not be ruled out for operative intervention should they have imaging evidence of lumbar stenosis superior to the expected affected level.

Nerve root compression due to lumbar spinal canal tophi: A case report and review of the literature.

Gout in the spine and adnexa is rare in clinical practice and can also be easily misdiagnosed, we reported a patient with nerve root compression due to lumbar gout stones in the lumbar spinal canal. A 51-year-old male was admitted to the hospital with lumbar pain with numbness in the left lower limb for more than 6 months. The physical examination showed that tenderness and percussion pain were present at L4-S1 spinous process. Straight leg raise test: 50° on the left side were positive. Laboratory tests showed that the sUA was 669 μmol/L, MRI of the lumbar spine showed that cystic T1WI low signal and T2WI mixed high signal shadows were seen in the spinal canal at the level of L4-L5. Combining with lab examinations, imaging examinations, and histopathological results, the patient was diagnosed with lumbar spinal canal tophi. After active improvement of all examinations, the patient underwent surgical treatment with decompression and internal fixation of the L4-L5 segment. After surgery, the patient's symptoms improved and muscle strength returned to normal. Among the 95 previously reported patients with lumbar gout, the ratio of men to women was 2.96:1, and the peak age group of incidence was 56 to 65 years. The onset of the disease was mainly in a single segment of the lumbar spine, with 34.41% of all cases occurring at the L4-L5 level. 61.05% of the patients had a history of gout attacks or hyperuricemia, and the most frequently involved site was the foot and ankle, followed by the wrist. Sixty-seven patients underwent surgical treatment, and 22 chose conservative treatment, with overall satisfactory results. The incidence of lumbar gout is low and relatively rare in the clinic and pathological biopsy is still the gold standard. Vertebral plate incision and decompression are often selected for surgical treatment, and whether to perform fusion should be comprehensively considered for the destruction of vertebral bone by gout and the reasonable selection of the extent of surgical resection. Whether choosing surgical treatment or conservative therapy, the control of uric acid levels should be emphasized.

Limbus Vertebral Fracture Presenting as Cauda Equina Syndrome Masquerading An Acute Disc Prolapse - A Rare Case Report and Review of Literature.

Limbus vertebral fracture is an uncommon injury described in adolescents. It refers to the separation of a bony fragment from the unfused ring apophysis of lumbar vertebral end plate. It usually presents with back pain with/without radiculopathy masquerading an acute disc prolapse. However, the presentation as acute cauda equina syndrome has seldom been reported. A 15-year-old male presented to the casualty with a history of acute-onset low back pain and bilateral lower limb radicular pain with weakness, after lifting of a heavy Indian musical instrument (Dholak). This was associated with urinary retention and numbness in perineal region. Examination revealed L5 and S1 weakness with absent ankle jerks bilaterally. Bulbocavernosus reflex was absent. Emergency magnetic resonance imaging imaging was done, which revealed a limbus fracture of cephalad part of L4 vertebral body with displaced fragment into the spinal canal causing compression of the cauda equina. Emergency surgery was done in the form of L3-L4 midline interlaminar microscopic decompression. The patient had complete neurological recovery including the bladder control within 1 month of surgery. The patient had no functional deficits during follow-up at 3 and6 months. Dynamic radiographs taken at the end of 6 months did not show any sign of instability. When an adolescent patient with no previous history of backpain presents with acute cauda equina syndrome, a possibility of limbus fracture should also be considered. Early diagnosis and surgical decompression in such cases can bring about complete neurological recovery and excellent clinical outcome.

Posterior lumbar interbody fusion for dysplastic lumbar spondylolisthesis with high-grade slippage in two adolescent siblings: two case reports.

Lumbar spondylolisthesis is reported to present with a familiar pattern, with the dysplastic type of spondylolysis being minor but more hereditary than the isthmic type. Siblings presenting during adolescence with neurological symptoms owing to high-grade dysplastic-type spondylolisthesis are rare. The older brother suffered from left leg pain and numbness and dysesthesia of the right posterior thigh and calf and could not walk without a crutch at the age of 15 years. He had canal stenosis with disc bulging and dysplastic bilateral facet joint at L5/S1. The L5 vertebral body was slipped anterior downward to S1, with a round-shaped S1 cranial endplate. We diagnosed dysplastic-type spondylolisthesis and performed posterior lumbar interbody fusion at L5/S with mild reduction and sublaminar wiring at L4/5. The younger brother had no neurological symptoms at age 14 years but suffered from bilateral lower leg numbness at age 18 years. He had canal stenosis with disc bulging at L4/5 and L5/S1 and dysplastic bilateral facet joint at L5/S1 with right pars defect. The L5 vertebral body was vertically displaced anterior to the S1 vertebral body, with an S1 round-shaped cranial endplate. We diagnosed dysplastic-type spondylolisthesis, and posterior lumbar interbody fusion at L4/5 and L5/S with reduction was performed. Their neurological symptoms of the lower legs disappeared, and interbody bone fusion was obtained. The surgical technique for high-grade dysplastic spondylolisthesis remains controversial in terms of in situ fusion versus reduction. We recommend that surgery be performed promptly at the end of bone maturation because neurological symptoms often appear at the end of bone maturation. Because high-grade slips are rare but siblings may be present, the sibling should also be screened when dysplastic spondylolisthesis is detected.

Anatomy, Back, Lumbosacral Trunk -- Surgical Considerations

Over 95% of lumbar disc herniations affect either the L4/L5 or L5/S1 disc spaces, or both. Patients commonly experience sharp, stabbing low back pain that radiates from the lower lumbar region down to the foot. [6] [7] [8] Nonsurgical management usually suffices in cases of lower extremity radiculopathy [9] [10] [11] and acute lumbar disc herniation. [8] The most common indication for surgical intervention is persistent, intractable pain despite at least 6 weeks of optimal conservative treatment. [12]

Lumbar spinal stenosis

Society and culture United States Under rules promulgated by Titles II and XVI of the United States Social Security Act, spinal stenosis is recognized as a disabling condition under Listing 1.04 C. The listing states: "Lumbar spinal stenosis resulting in neurogenic claudication, established by findings on appropriate medically acceptable imaging, manifested by chronic nonradicular pain and weakness, and resulting in inability to ambulate effectively, as defined in 1.00B2b." The regulation is written specifically for lumbar stenosis. References External links Geriatrics Spinal cord disorders Bones of the vertebral column

Lumbar spinal stenosis

Among people with lower-extremity pain in combination with back pain, lumbar stenosis as the cause is two times more likely in those older than 70 years of age while in those younger than 60 years it is less than half as likely. The character of the pain is also useful for diagnosis. When the discomfort does not occur while seated, the likelihood of lumbar spinal stenosis increases considerably, around 7.4 times. Other features increasing the likelihood of lumbar stenosis are improvement in symptoms on bending forward (6.4 times), pain that occurs in both buttocks or legs (6.3 times), and the presence of neurogenic claudication (3.7 times). On the other hand, the absence of neurogenic claudication makes lumbar stenosis much less likely as the explanation for the pain. Causes

Spinal disc herniation

Lumbar disc herniations occur in the back, most often between the fourth and fifth lumbar vertebral bodies or between the fifth and the sacrum. Here, symptoms can be felt in the lower back, buttocks, thigh, anal/genital region (via the perineal nerve), and may radiate into the foot and/or toe. The sciatic nerve is the most commonly affected nerve, causing symptoms of sciatica. The femoral nerve can also be affected and cause the patient to experience a numb, tingling feeling throughout one or both legs and even feet or a burning feeling in the hips and legs. A herniation in the lumbar region often compresses the nerve root exiting at the level below the disc. Thus, a herniation of the L4–5 disc compresses the L5 nerve root, only if the herniation is posterolateral. Cervical disc herniation

Lumbar vertebrae

Most individuals have five lumbar vertebrae, while some have four or six. Lumbar disorders that normally affect L5 will affect L4 or L6 in these latter individuals. Segmental movements The range of segmental movements in a single segment is difficult to measure clinically, not only because of variations between individuals, but also because it is age and sex dependent. Furthermore, flexion and extension in the lumbal spine is the product of a combination of rotation and translation in the sagittal plane between each vertebra. Ranges of segmental movements in the lumbar spine (White and Punjabi, 1990) are (in degrees): Congenital anomalies Congenital vertebral anomalies can cause compression of the spinal cord by deforming the vertebral canal or causing instability.

InternalMed_Harrison

The straight leg–raising (SLR) maneuver is a simple bedside test for nerve root disease. With the patient supine, passive flexion of the extended leg at the hip stretches the L5 and S1 nerve roots and 113 CHAPTER 22 Back and Neck Pain 4th Lumbar vertebral body 5th Lumbar vertebral body 4th Lumbar pedicle L4 root Protruded L4-L5 disk L5 Root S1 Root S2 Root Protruded L5-S1 disk FIguRE 22-3 Compression of L5 and S1 roots by herniated disks. (From AH Ropper, MA Samuels: Adams and Victor’s Principles of Neurology, 9th ed. New York, McGraw-Hill, 2009; with permission.) the sciatic nerve. Passive dorsiflexion of the foot during the maneuver adds to the stretch. In healthy individuals, flexion to at least 80° is normally possible without causing pain, although a tight, stretching sensation in the hamstring muscles is common. The SLR test is positive if the maneuver reproduces the patient’s usual back or limb pain. Eliciting the SLR sign in both the supine and sitting positions can help

Lumbar Degenerative Disk Disease -- History and Physical

The straight leg raise (SLR) test consists of a supine patient having his/her fully extended leg passively stretched from 0 to about 80 degrees. The onset of radiating back pain in either leg supports a diagnosis of a stenotic canal. A herniation compressing the L5 nerve root will present as a weakness of ankle dorsiflexion and an extension of the great toe. This deficit also may diminish the Achilles tendon reflex. L4 radiculopathy may present with weakness in the quadriceps and a decreased patellar tendon reflex. Documentation is paramount, as these initial findings likely will be used as a baseline for all future evaluations.

Anatomy, Back, Lumbar Spine -- Clinical Significance

Compression, injury, or irritation of the lumbar spinal nerve roots can occur from multiple potential sources. Most commonly, this occurs as a consequence of the degenerative cascade or an acute disc herniation. Lumbar radiculopathy (aka sciatica) describes the constellation of symptoms resulting from lumbar nerve compression. Individuals present with variable degrees of radiating pain, paresthesia (numbness/tingling), and weakness in the lower extremities. Lumbar stenosis is a condition in which the narrowing of the spinal canal occurs. This narrowing is usually secondary to degenerative spondylosis and spondylolisthesis. Classically individuals present with low back and/or lower extremity pain/paresthesias, which worsen with lumbar extension, prolonged standing, and ambulation. The pathophysiology appears to be due to mechanical compression of the lumbosacral spinal nerve roots resulting in ischemia. [16] [17]

InternalMed_Harrison

PART 2 Cardinal Manifestations and Presentation of Diseases FIguRE 22-1 Vertebral anatomy. (From A Gauthier Cornuelle, DH Gronefeld: Radiographic Anatomy Positioning. New York, McGraw-Hill, 1998; with permission.) Radicular pain is typically sharp and radiates from the low back to a leg within the territory of a nerve root (see “Lumbar Disk Disease,” below). Coughing, sneezing, or voluntary contraction of abdominal muscles (lifting heavy objects or straining at stool) may elicit the radiating pain. The pain may increase in postures that stretch the nerves and nerve roots. Sitting with the leg outstretched places traction on the sciatic nerve and L5 and S1 roots because the nerve passes posterior to the hip. The femoral nerve (L2, L3, and L4 roots) passes anterior to the hip and is not stretched by sitting. FIguRE 22-2 Spinal column. (From A Gauthier Cornuelle, DH Gronefeld: Radiographic Anatomy Positioning. New York, McGraw-Hill, 1998; with permission.)

Spinal Stenosis -- History and Physical

Stenosis in the lumbar spine can lead to neurogenic claudication, myeloradiculopathy symptoms, sensory disturbances, motor weakness, and pathologic reflexes. Patients will present with complaints of cramping pain in the leg, calf, and or buttocks. They might report an increase in pain with walking or standing for prolonged periods and relief when sitting or leaning forward while using a shopping cart. [9] Disk herniation is most common at the L4-5 and L5-S1 levels. A herniated disk at L5-S1 can lead to plantarflexion weakness, decrease sensation in the lateral foot, and cause pain in the posterior leg. A disk herniation at L4-5 can lead to a foot drop and numbness in the large toe web and dorsal aspect of the foot. Lastly, an L3-4 disk herniation can lead to knee extension weakness, numbness in the medial foot, and pain in the anterior thigh.

Lumbar Disc Herniation -- History and Physical

L5 nerve root exits at the L5-S1 foramina. When compressed by a herniated disc, it causes back pain that radiates into the buttock, lateral thigh, lateral calf, the dorsum of the foot, and the great toe. Sensory loss is present on the web space between the big toe and second toe, the dorsum of the foot, and lateral calf. There is a weakness in hip abduction, knee flexion, foot dorsiflexion, big toe dorsiflexion, foot inversion, and eversion. Patients present with decreased semitendinosus/semimembranosus reflex. Weakness in foot dorsiflexion makes it challenging to walk on the heels. Chronic L5 radiculopathy may cause atrophy of the extensor digitorum brevis and the tibialis anterior of the anterior leg.

Tophaceous gout causing lumbar stenosis: A case report.

Gout in the spine is very rare. The clinical symptoms of the spinal gout are various and lack of specificity. The authors report a case of spinal gout causing lumbar stenosis. We never find such wide-invasive spinal gouty lesion in the published studies. A 68-year-old male had low back pain radiating to bilateral lower limbs, accompanying with intermittent claudication that lasted for 3 months and aggravated 5 days ago. Spinal gout, lumbar stenosis. The patient underwent L2-L4 laminectomy, L2/3 L3/4 an d L4/5 discectomy and transforaminal lumbar interbody fusion with pedicle screw fixation. Dual-energy computed tomography detected extensive tophaceous deposits in L1/2 L2/3 L3/4 and L4/5 lumbar discs as well as the posterior column, especially L2-L3 and L4-L5 facet joints. During the surgery, we found a mass of chalky white material at the posterior column of L3 to L5 vertebral bodies, which also involved the intervertebral discs. Pathological examination confirmed the diagnosis of spinal gout. Although spinal gout is thought to be rare, the diagnosis should be considered if the patient had severe back pain and a history of gout. Dual-energy computed tomography is highly recommended for these patients.

Surgery_Schwartz

to provide crucial collateral flow in maintaining lower limb viabil-ity. It must be emphasized, however, that patients should be subjected to angiography only if their symptoms warrant surgi-cal intervention.Differential DiagnosisDegenerative hip or spine disease, lumbar disk herniation, spinal stenosis, diabetic neuropathy, and other neuromuscular problems can produce symptoms that may be mistaken for vas-cular claudication. Such cases can be distinguished from true claudication by the fact that the discomfort from neuromuscular problems is often relieved by sitting or lying down, as opposed to cessation of ambulation. In addition, complaints that are Table 23-13Clinical outcome of renal artery stent placement in the treatment of renovascular hypertension and renal insufficiencyAUTHORYEARPATIENT NO.TECHNICAL SUCCESS (%)FOLLOW-UP (MONTHS)RENAL INSUFFICIENCY (%)RENOVASCULAR HYPERTENSION (%)COMPLICATION (%)RESTENOSIS

Lumbar spinal stenosis.

Symptoms for spinal stenosis apparently result from an incongruity between the capacity and contents of the spinal nerve passages. These symptoms are most frequently seen in men in their fifth or sixth decade of life. Spinal extension generally exacerbates the claudication-type symptoms (lower-extremity pain and paresthesia), whereas spinal flexion diminishes these symptoms. Differential diagnosis is needed to rule out vascular claudication due to atherosclerosis. Decisions regarding surgery should be made based not only on diagnostic imaging but also on a thorough history and clinical examination.

Neurology_Adams

Herniation of Lumbar Intervertebral Discs (Table 10-1) This condition is a major cause of severe and chronic or recurrent low back and leg pain. It occurs mainly during the third and fourth decades of life when the nucleus pulposus is still gelatinous. The disc between the fifth lumbar or first sacral vertebrae (L5-S1) is most often involved, and, with decreasing frequency, that between the fourth and fifth (L4-L5), third and fourth (L3-L4), second and third (L2-L3), and—quite infrequently—the first and second (L1-L2) lumbar vertebrae. Disc disease is relatively rare but well described in the thoracic portion of the spine. It is frequent in the cervical spine, especially at the fifth and sixth and the sixth and seventh cervical vertebrae (see further on).

Traumatic burst fracture in a patient with a lumbar artificial disc.

Lumbar disc arthroplasty is now a common treatment for lumbar degenerative disc disease. Whereas the immediate and delayed complications in patients with artificial lumbar discs are well reported, the durability of artificial disc hardware after severe spine trauma is unknown. The authors describe the management of a rare case of a traumatic lumbar burst fracture in a patient who had undergone disc arthroplasty. This 31-year-old male contractor had undergone placement of an L4-5 Charité artificial disc (DePuy Spine) and L5-S1 anterior lumbar fusion 10 months before he fell from a roof and sustained a traumatic L-3 burst fracture with significant canal compromise and cauda equina injury. Despite the considerable compressive load on his spine, the artificial disc (L4-5) remained intact without any radiological signs of hardware failure, and the vertebrae above (L-4) and below (L-5) the artificial disc had no signs of injury. For the L-3 burst fracture the patient underwent an open decompressive laminectomy at L2-3 and posterior fusion with instrumentation from L-2 to L-4. At 24 months postinjury, he had returned to full work activities as a contractor with minimal back pain and mild right lower-extremity sensory changes and weakness left over from the trauma. The total disc arthroplasty at L4-5 is functional and has preserved motion, and there is a solid fusion at L2-4 and L5-S1. This case demonstrates that a lumbar artificial disc can tolerate a significant load from trauma and remain functional without hardware failure even after a traumatic burst fracture at the adjacent lumbar vertebral body and shows the successful treatment of this fracture, with posterior fusion preserving the motion of an artificial disc.

Clinical features of lumbar spinal stenosis.

In contrast with patients with herniations of the nucleus pulposus, those with spinal stenosis experience onset of symptoms at a slightly older age; more males are affected than females. The symptoms tend to be somewhat more chronic, and therefore, the patients will have symptoms of back pain for a longer period of time before developing radiating root pains and will not come to surgical treatment until relatively late. Bilateral root symptomatology is more common although examination shows multiple nerve root involvement only slightly more frequently as well as involvement of the L1 to L4 nerve roots. The spinal movements tend to be somewhat better and straight leg raising tests are usually symmetrical and somewhat less restricted in those patients than in the acute disk syndrome. Postfusion and post-chemonucleolysis spinal stenosis will, of course, have the symptomatology of the initial problem, but their recurrent problems would tend to parallel those of spinal stenosis rather than disk herniation.

Spinal disease

Lumbar spinal stenosis is classified as a narrowing of the spinal canal in the lumbar region of the vertebrae. This may lead to compression of the nerve root of the spinal cord and result in pain of the lower back and lower extremities. Other symptoms include impaired walking and a slightly stooped posture due to loss of disc height and bulging of the disc. Lumbar spinal stenosis is very prevalent with 9.3% of the general population producing symptoms and the number is continuing to rise in patients older than 60. It's generally an indication for spinal surgery in patients older than 65 years of age. However, there is a myth and fear among most patients that only surgery is the cure for such conditions and spine surgery is very risky. There are many non-surgical treatments available to prevent, halt and even reverse many spine diseases. Also, some surgery patients can be operated on in a daycare procedure or with minimum length of stay in hospital, with statistically good outcomes.

Firearm bullet settling into the lumbar spinal canal without causing neurological deficit: A report of two cases.

Uncertainty still exists regarding the treatment of the patients presenting with gunshot wounds to the spine. Neurological insults, cerebrospinal fluid fistula, infection, lead or copper toxicity, migration of bullets, and spinal instability are included among the common challenging issues. An 18-year-old woman was admitted with low back pain following a gunshot injury five days ago. She was neurologically intact. Radiological examinations showed that a bullet was settled in L4-5 disc space. The bullet was removed with a unilateral L4-5 partial hemilaminectomy and discectomy from the left side. The second case was of a 29-year-old man admitted with radiating leg pain on the right side following a gunshot injury from his left side of lower back four months ago. He had only positive straight leg raising test. Radiological studies showed two bullets, one was in the psoas muscle on the left side and the other was in spinal canal that had caused a burst fracture of the L5 vertebra. Following L5 laminectomy and bilateral L5-S1 facetectomy, the bullet was removed from the spinal canal and L5-S1 transpedicular posterior stabilization was performed. The postoperative period of both patients was unremarkable. Bullet settling into the lumbar spinal canal without causing neurological deficit may require surgical intervention. Removal of bullets provided not only pain relief in both the cases but also prevented future complications such as migration of the bullets, plumbism, and neuropathic pain and instability.

Clinical Presentations of Lumbar Disc Degeneration and Lumbosacral Nerve Lesions.

Lumbar disc degeneration is defined as the wear and tear of lumbar intervertebral disc, and it is mainly occurring at L3-L4 and L4-S1 vertebrae. Lumbar disc degeneration may lead to disc bulging, osteophytes, loss of disc space, and compression and irritation of the adjacent nerve root. Clinical presentations associated with lumbar disc degeneration and lumbosacral nerve lesion are discogenic pain, radical pain, muscular weakness, and cutaneous. Discogenic pain is usually felt in the lumbar region, or sometimes, it may feel in the buttocks, down to the upper thighs, and it is typically presented with sudden forced flexion and/or rotational moment. Radical pain, muscular weakness, and sensory defects associated with lumbosacral nerve lesions are distributed on lower extremities, the buttock, lower abdomen, and groin region. A lumbosacral plexus lesion presents different symptoms in the territories of the lumbar and sacral nerves. Patients with lumbar plexus lesion clinically present with weakness of hip flexion, knee extension, thigh adduction, and sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg, while sacral plexus lesion presents clinical symptoms at nerve fibers destined for the sciatic nerve, common peroneal nerve, and pudendal nerve. Weakness of ankle inversion, plantar flexion, and foot drop are the main clinical manifestations of the sacral plexus lesion area. Numbness and decreased sensation are also present along the anterolateral calf and dorsum of the foot. On examination, foot eversion is usually stronger than foot dorsiflexion. The patients may also present with pain and difficulty of bowel movements, sexual dysfunction assessments, and loss of cutaneous sensation in the areas of the anal canal, anus, labia major, labia minor, clitoris, penis, and scrotum.

Lumbar vertebral body and pars fractures following laminectomy.

A 56-year-old alcoholic male incurred L5 vertebral body and bilateral L4 pars fractures with progressive L4 on L5 anterolisthesis following low-energy falls while intoxicated. Recently, he had a L3-S1 laminectomy for lumbar spinal stenosis with claudication. Preoperative imaging and radiographs were negative for pars defects and instability, so an isolated decompressive surgery was performed. Following low-energy falls, his outpatient work-up revealed fractures through the bilateral L4 pedicles and posterior third of L5 vertebral body, with recurrence of axial back pain and bilateral lower extremity radiculopathy. He underwent revision decompression from L4-S1 and posterior instrumented fusion with transforaminal lumbar interbody fusion performed at each revised level. His axial back pain and radiculopathy improved postoperatively. Instability of a lumbar spine fracture pattern can be due to the remote or prior iatrogenic disruption of the posterior ligamentous complex. Our patient benefitted from surgery and his low back pain was resolved.

Lumbar Spinal Stenosis -- History and Physical

Some patients with LSS may be asymptomatic and have a normal neurologic examination. Other individuals with asymptomatic LSS may have neurologic deficits due to superimposed lumbar radiculopathy. The Valsalva maneuver often does not exacerbate LSS-related radicular pain as it does in IV disk prolapse. Only 10% of patients present with a positive straight leg raise test. [24] Pedal pulses should also be checked during the physical exam to rule out vascular claudication. A patient who can perform a five-repetition sit-to-stand (5R-STS) test in 10.4 seconds may be considered to have no functional impairment. [25]

Vertical split fracture of the vertebral body following oblique lumbar interbody fusion: A case report.

Oblique lumbar interbody fusion (OLIF) is an effective and safe surgical technique widely used for treating spondylolisthesis; however, its use is controversial because of several associated complications, including endplate injury. We report a rare vertebral body fracture following OLIF in a patient with poor bone quality. A 72-year-old male patient visited our clinic for 2 years with lower back pain, leg radiating pain, and intermittent neurogenic claudication. Lumbar magnetic resonance imaging revealed L4-5 stenosis. We performed OLIF with percutaneous pedicle screw fixation and L4 subtotal decompressive laminectomy. We resected the anterior longitudinal ligament partially for anterior column release and inserted a huge cage to maximize segmental lordosis. No complications during and after the operation were observed. Further, the radiating pain and back pain improved, and the patient was discharged. Two weeks after the operation, the patient visited the outpatient department complaining of sudden recurred pain, which occurred while going to the bathroom. Radiography and computed tomography revealed a split fracture of the L5 body and an anterior cage displacement. In revision of OLIF, we removed the dislocated cage and filled the bone cement between the anterior longitudinal ligament and empty disc space. Further, we performed posterior lumbar interbody fusion L4-5, and the screw was extended to S1. After the second surgery, back pain and radiating pain in the left leg improved, and he was discharged without complications. In this case, owing to insufficient intervertebral space during L4-5 OLIF, a huge cage was used to achieve sufficient segmental lordosis after anterior column release, but a vertebral body coronal fracture occurred. In patients with poor bone quality and less flexibility, a huge cage and over-distraction could cause a vertebral fracture; hence, selecting an appropriate cage or considering a posterior approach is recommended.

InternalMed_Harrison

Nerve root injury (radiculopathy) is a common cause of neck, arm, low back, buttock, and leg pain (see Figs. 31-2 and 31-3). The nerve roots exit at a level above their respective vertebral bodies in the cervical region (e.g., the C7 nerve root exits at the C6-C7 level) and below their respective vertebral bodies in the thoracic and lumbar regions (e.g., the T1 nerve root exits at the T1-T2 level). The cervical nerve roots follow a short intraspinal course before exiting. By contrast, because the spinal cord ends at the vertebral L1 or L2 level, the lumbar nerve roots follow a long intraspinal course and can be injured anywhere from the upper lumbar spine to their exit at the intervertebral foramen. For example, disk herniation at the L4-L5 level can produce not only L5 root compression, but also compression of the traversing S1 nerve root (Fig. 22-3). The lumbar nerve roots are mobile in the spinal canal, but eventually pass through the narrow lateral recess of the spinal canal and

Lordosis

Diagnosis Measurement and diagnosis of lumbar hyperlordosis can be difficult. Obliteration of vertebral end-plate landmarks by interbody fusion may make the traditional measurement of segmental lumbar lordosis more difficult. Because the L4–L5 and L5–S1 levels are most commonly involved in fusion procedures, or arthrodesis, and contribute to normal lumbar lordosis, it is helpful to identify a reproducible and accurate means of measuring segmental lordosis at these levels. A visible sign of hyperlordosis is an abnormally large arch of the lower back and the person appears to be puffing out his or her stomach and buttocks. Scanning

[Lumbar canal stenosis. Retrospective study of 158 operated cases].

The authors report the results of a retrospective study of 158 lumbar spinal stenosis (LSS), all operated (111 degenerative, 26 congenital, 21 mixed). Eighty seven percent of the patients had a low-back pain and 81.6% a radicular pain. Only 57.6% of them had a polyradicular claudication. A neurological deficit (motor, sensitive, or involving sphincters) was present in 36.6% of cases. A myelographic block was noted in 23.4% of cases, and in 20.3% a spondylolisthesis with an intact neural arch was found. Surgery consisted of a posterior lateral spinal canal calibration, sometimes associated with a ventral canal calibration (via the posterior route) (6.3%), and/or excision of a disc herniation at one (47.5%) or two levels (3.8%). Mean follow-up after surgery was 7.8 months. The global result was good or excellent in 75.2% of cases. Radicular pain was relieved in 89.1% of cases, and polyradicular claudication in 90.1% of cases. Neurological deficit improved in 50.6% of cases. In only 59.8% of cases relief of low-back pain was achieved. Statistically low-back pain (lasting for over 2 years) improved less, but a preoperative spondylolisthesis didn't influence the quality of the result regarding this symptom. Semiology, pathophysiology, and surgery particularly regarding spine stability are discussed.

Back pain

Spinal disc disease Spinal disc disease occurs when the nucleus pulposus, a gel-like material in the inner core of the vertebral disc, ruptures. Rupturing of the nucleus pulposus can lead to compression of nerve roots. Symptoms may be unilateral or bilateral, and correlate to the region of the spine affected. The most common region for spinal disk disease is at L4–L5 or L5–S1. The risk for lumbar disc disease is increased in overweight individuals due to the increased compressive force on the nucleus pulposus, and is twice as likely to occur in men. A 2002 study found that lifestyle factors such as night shift work and lack of sporting activity can also increase the risk of lumbar disk disease.

Comparison of radicular symptoms caused by lumbar disc herniation and lumbar spinal stenosis in the elderly.

Comparative study using combined data from 2 prospective cohort studies. To expose the differences between the clinical characteristics of neurogenic claudication from magnetic resonance image-documented lumbar spinal stenosis (LSS) and lumbosacral radicular syndrome from acute, magnetic resonance image-documented, lumbar disc herniation (LDH). LSS and LDH are the common lumbar disorders that produce lower extremity pain. Though known factors such as pain induced by walking for LSS and the rapid onset of symptoms for LDH are useful for differentiating these disorders, exploration of differences in other factors has received limited study. This study included participants aged 60 yr or older from 2 previous studies. One examined walking limitations caused by LSS and the second the natural history of LDH in elderly adults. The clinical features of both groups were compared by calculating means, medians, and standard deviations for continuous variables, and frequencies for categorical variables. χ test was used to explore differences between LSS and LDH for categorical variables, and Student t test or Mann-Whitney test for continuous variables. Participants with LSS had more medical comorbidity, less intense leg pain, and less disability than those with LDH. Leg pain was more common in the anterior thigh, anterior knee and shin in LDH, and in the posterior knee in LSS. Trunk flexion was more impaired in LDH. Positive straight leg raising and femoral stretch signs were common in LDH, and rare in LSS. Abnormal Achilles reflexes were noted more frequently in LSS. In addition to established factors, greater leg pain intensity, greater disability, and pain in the anterior leg are more common in the elderly with LDH than in the elderly with LSS. Normal trunk flexion, absence of nerve root tension signs and abnormal Achilles reflexes are more common in LSS. 3.