George M. Kushner, DMD, MD

• Professor of Oral and Maxillofacial Surgery
• University of Louisville School of Dentistry
• Louisville, Kentucky

Acute lesions may be self-limited and resolve within a few days to a few weeks (especially in children) unless cold exposure persists herbals vitamins buy himplasia without a prescription, the lesions become infected herbals supplements buy 30caps himplasia with visa, or the skin is broken by iatrogenic causes such as self-treatment with severe heat or vigorous massage herbalshopcompanynet discount 30caps himplasia overnight delivery. Initially herbals in the philippines generic 30caps himplasia amex, pernio may start late in the fall or early winter and resolve in early spring herbs unlimited purchase generic himplasia pills. If left untreated rumi herbals chennai discount himplasia 30caps mastercard, the lesions of pernio may start earlier in the cold season and resolve later, until eventually all seasonal variation is lost. Pernio tends to be more severe in adults and may, if left untreated, eventually cause macrovascular occlusive disease. Note brown and yellow flaking lesion on thumb (A) and healing lesions on index and ring fingers (B). Some authors suggested that most lupus pernio patients have lesions on the hands, but this anatomical localization was not a differentiating factor between idiopathic pernio and lupus pernio according to others. Erythrocyanosis affects adolescent girls and young women and typically involves the lower extremities. Some have classified this as the "nodular chronic form" of pernio; lesions take on a swollen, dusky red appearance. A comprehensive history and complete physical exam are the primary means by which the diagnosis of pernio can be correctly established. Chronological correlation between nonfreezing cold and onset of typical lesions that improve with onset of warm weather should strongly suggest the diagnosis. These lesions typically disappear when the weather warms up at the beginning of spring. However, in some chronic cases in which the lesions do not disappear in warm weather, or in which the lesions cause severe pigmentation and disfiguration of the lower part of the leg, the diagnosis may be more difficult. The main obstacle to establishing the diagnosis of pernio is unfamiliarity of the healthcare provider with the disease. Since many of the dermatological manifestations associated with pernio overlap with other serious diseases, it is not uncommon for pernio patients to be subjected to unnecessary investigations and suffer needless delay in proper treatment. Because the diagnosis of pernio is a clinical diagnosis, sophisticated laboratory tests are often not needed, but it is important to rule out other entities that can mimic pernio. Atheromatous emboli (blue toe syndrome) is the most challenging diagnostic entity to differentiate from pernio because similar lesions may be present in each disorder (see Chapter 45). When the history of cold exposure is uncertain and in patients with established or suspected atherosclerosis, imaging studies often are warranted to demonstrate atheroma in the aorta or iliac vessels. A biopsy of these lesions showing characteristic cholesterol clefts establishes the diagnosis of atheromatous emboli. Erythema induratum (Bazin disease) is often but not always a cutaneous form of tuberculosis that affects adolescent girls and is manifested by nodular ulcerating lesions of the calves. Although the nodules of nodular vasculitis are extremely painful, they rarely ulcerate. Erythema nodosum may be differentiated from pernio in that it may be associated with fever, arthralgias, malaise, and an underlying disease. Cold panniculitis is another important entity characterized by painful nodules that appear on the skin after cold exposure and can be reproduced by application of an ice cube. Lack of the systemic manifestations and laboratory abnormalities that occur in leukocytoclastic vasculitis and the relation of the lesions to cold exposure in pernio serve to separate these two conditions. Treatment Since the primary trigger for development of pernio is cold exposure, prevention is the mainstay of management. Working in a damp cold basement or living in a poorly heated apartment may necessitate change of profession or moving to a properly heated residence. Patients do not always volunteer information about the climate of their residence and workplace, so the physician may need to ask specifically about the quality of heating systems and the degree of humidity present. Adequate body insulation with gloves, stockings, footwear, and headwear may be needed. As is the case in the treatment of Raynaud phenomenon, the entire body must be kept warm. A dihydropyridine calcium channel blocker, such as nifedipine, may be quite effective in patients with pernio. In a double-blind placebo-controlled randomized crossover pilot study, Dowd et al. In addition, the pain disappeared within 5 days in the treated group, compared to 20 to 25 days in the group receiving placebo. Thus, administration of an oral agent such as nifedipine may cause symptomatic hypotension. In these circumstances, I recommend the use of topical nifedipine, 5% in non-ionic cream, applied to the feet or toes twice a day. Other agents such as topical nitroglycerin, oral pentoxifylline, and hydroxychloroquine have been used with variable degrees of success. Despite speculation that it may enhance resolution of active lesions and provide subjective improvement, sympathectomy does not prevent recurrence of new lesions and has little effect if any on pigmentation and thickness at the sites of perniotic lesions. Given the controversy and lack of prospective studies, routine use of these agents is not recommended. Epidemiological patterns of perniosis, and its association with systemic disorder. Vasomotor microcirculatory insufficiency: observations on nonfreezing cold injury of the mouse ear. Vasospasm is a consistent finding in pernio (chilblains) and a possible clue to pathogenesis. Perniosis (chilblains) of the thigh: report of five cases, including four following river crossings. Observations on some normal and injurious effects of cold upon the skin and underlying tissues: chilblains and allied conditions. Chilblains and antiphospholipid antibodies: report of four cases and review of the literature. Adult perniosis and cryoglobulinemia: a retrospective study and review of the literature. Clinical and histopathologic features and immunologic variables in patients with severe chilblains. Pernio of the hips in young girls wearing tight-fitting jeans with a low waistband. The treatment of chilblains with nifedipine: the results of a pilot study, a double-blind placebo-controlled randomized study and a longterm open trial. Nifedipine vs placebo for treatment of chronic chilblains: a randomized controlled trial. Treatment of primary perniosis with oral pentoxifylline (a double-blind placebo-controlled randomized therapeutic trial). Common provoking factors include cancer, surgery, trauma, and immobilization, and together these account for about 50% of cases. Other risk factors include older age, obesity, pregnancy, kidney disease, sickle cell trait, and use of exogenous estrogen or other hormonal medications. However, the differences in findings from these studies with varied designs remain unexplained. Data is based on appearance of diagnosis codes in the principal position (blue; reason for the hospital stay) or any position (orange) in the list of discharge diagnosis codes. Heart disease and stroke statistics-2018 update: a report from the American Heart Association. One study reported a decreasing age-adjusted, in-hospital case fatality rate from 12. It is important to consider that the impact of combinations of risk factors tends to be at least additive and often multiplicative, such that the more factors present, the higher the risk. For example, hip and knee arthroplasties have doubled in the Netherlands between 1995 and 2010. As such, with the graying of the population, we could anticipate an increase in incidence over time. Between 1990 and 2000, the obesity prevalence in the United States rose from 10% to 25%. If the obesity rate had remained unchanged there would have been 21,000 events attributable to obesity in 2000 rather than an estimated 52,500 cases. It can also be expected that the prevalence of cancer will increase in the upcoming years. However, these risk factors are generally persistent risk factors, so consideration and understanding is important, especially for researchers. About 8% of African Americans are carriers of the sickle cell trait, the heterozygous form of sickle cell disease. Guidelines recommend that clinicians tailor anticoagulation duration based of the risk benefit ratio and patient preference. Correct diagnosis and classification are critical to designing treatment plans for patients since many patients are treated with long-term anticoagulants after a single event. Established and emerging risk factors discussed above should be considered by clinicians when they educate their patients. Heart disease and stroke statistics-2018 update: a report from the American Heart Association. Racial and regional differences in venous thromboembolism in the United States in 3 cohorts. Incidence of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism: a contemporary view of the published literature. Current incidence of venous thromboembolism and comparison with 1998: a community-based study in Western France. Time trends in incidence rates of venous thromboembolism in a large cohort recruited from the general population. Time trends in pulmonary embolism in the United States: evidence of overdiagnosis. Time trends and case fatality rate of in-hospital treated pulmonary embolism during 11 years of observation in Northwestern Italy. Subsegmental pulmonary embolism diagnosed by computed tomography: incidence and clinical implications. Body size measures, hemostatic and inflammatory markers and risk of venous thrombosis: the Longitudinal Investigation of Thromboembolism Etiology. A clinical prediction model for cancer-associated venous thromboembolism: a development and validation study in two independent prospective cohorts. Taller height as a risk factor for venous thromboembolism: a Mendelian randomization meta-analysis. Global prevalence of chronic kidney disease - a systematic review and meta-analysis. Association of mild to moderate chronic kidney disease with venous thromboembolism: pooled analysis of five prospective general population cohorts. Embolic burden of incidental pulmonary embolism diagnosed on routinely performed contrast-enhanced computed tomography imaging in cancer patients. Dalteparin thromboprophylaxis in cancer patients at high risk for venous thromboembolism: a randomized trial. Risk of recurrent venous thromboembolism and mortality in patients with cancer incidentally diagnosed with pulmonary embolism: a comparison with symptomatic patients. Incidental versus symptomatic venous thrombosis in cancer: a prospective observational study of 340 consecutive patients. Venous thromboembolism prophylaxis and treatment in patients with cancer: American Society of Clinical Oncology clinical practice guideline update 2014. Patients present with a variety of symptoms that can also be attributed to other clinical conditions. Imaging and complimentary laboratory studies also assist in the risk stratification and aid in treatment decision-making. The Virchow triad of hypercoagulability, endothelial injury, and venous stasis holds true for more than 150 years after its initial description. Extremity discomfort was reported in 70% of outpatients, but only 37% of inpatients. The physical exam is often notable for swelling and tenderness, but warmth and erythema can also be present. Signs and symptoms tend to be more common in those patients diagnosed as an outpatient compared to those hospitalized at the time of diagnosis, with over 10% of inpatients having no signs or symptoms and compared to only 2% of outpatients. Phlegmasia alba dolens is the early stage of decreased perfusion as the leg will appear white. This may progress further to become phlegmasia cerulea dolens-frank venous gangrene of the limb. In the most severe cases, patients can present with hypotension, shock, active cardiac arrest, or respiratory failure. Overall, clinical signs and symptoms in isolation have poor specificity, thus further evaluation of risk factors and clinical risk stratification is required. Clinical decision scores are valuable tools in the urgent care and emergency department setting but appear to be less helpful in the primary care setting. Arterial blood gases may demonstrate hypoxemia, increased alveolar to arterial gradient, and a respiratory alkalosis secondary to hypocapnia, but also may be normal. Ultrasound offers accurate imaging with no exposure of radiation or iodinated contrast to the patient. Blunted peak velocities, especially if different than the contralateral extremity, are suggestive of more proximal obstruction. There is slightly increased echogenicity present within the lumen of the femoral vein which is suggestive of thrombus. Because of the subclavicular location of the subclavian vein, compression cannot be used to evaluate for thrombus; however, color duplex can assist and demonstrate lack of flow in a segment of the vein (red arrow). Though rarely performed, invasive contrast venography can still be used if other imaging remains inconclusive. The frequency of nondiagnostic studies has decreased with these technological advancements.

Prothrombin 20210A is a mutation (G to A substitution) in the prothrombin gene at nucleotide 20210 herbals interaction with antihistamines order himplasia 30caps with visa, resulting in increased levels of plasma prothrombin himalaya herbals products generic 30caps himplasia otc. Congenital protein C deficiency may be transmitted as an autosomal dominant or recessive trait and has a prevalence of 1:200 to 1:500 zigma herbals purchase himplasia in united states online. Functional and immunologic assays are available to establish the diagnosis of protein C deficiency Healthy adults have protein C antigen levels ranging from 70% to herbs native to outland cheap himplasia online mastercard. Patients with antigen levels less than 55% are likely to have heterozygous protein C deficiency ganapathy herbals cheap himplasia 30caps online. Approximately 60% of the total protein S circulates bound to C4b complement-binding protein aasha herbals order himplasia 30 caps otc. Histories of patients with congenital protein S deficiencies are similar to those of patients with protein C deficiency although arterial, thromboses also have been described in patients with protein S deficiency Protein S can. Consequently plasma levels may be decreased in patients with hepatic, insufficiency Acquired protein C and protein S deficiencies can also occur with warfarin. Because C4b is also an acute-phase reactant, inflammatory conditions can increase C4b levels, causing a decrease in free protein S and an increased tendency toward thrombosis. Because warfarin-induced skin necrosis is more likely to occur in patients with protein C deficiency heparin therapy, should overlap with the first 4 or 5 days of warfarin therapy and large loading dosages of, warfarin should be avoided. Longer-term treatment with warfarin is effective in the prevention of recurrent venous thromboembolic episodes in patients with protein C and protein S deficiencies. Abnormalities of fibrinogen and fibrinolysis include dysfibrinogenemias, which may impair any of the steps involved in the generation and cross-linkage of fibrin. Acquired Prothrombotic Conditions Many clinical disorders predispose to thrombosis by activating the coagulation system or causing platelet aggregation. Soft tissue trauma, thermal injuries, and operative dissection all predispose to thrombosis through the release of tissue factor and activation of the extrinsic coagulation pathway. Gram-positive bacteria may directly cause platelet aggregation and subsequent thrombosis. As many as 11% of patients with malignancies have venous thromboembolic complications. Oral contraceptives and hormonal replacement therapy are also associated with an approximately threefold increased risk, which is conferred immediately and is reversible. In vivo, antiphospholipid antibodies may promote thrombosis by interfering with the activation of protein C. Clinical manifestations of the antiphospholipid syndrome may include venous and arterial thromboses (coronary cerebral) and recurrent fetal loss. As many as 50% of patients who are positive for lupus anticoagulants and undergo vascular surgical procedures develop thrombotic complications. However, thrombocytopenia is not a prerequisite for the development of thrombotic complications. The development of thrombocytopenia or a significantly decreased platelet count while receiving heparin 2. Patients with a 4Ts score 3 may continue heparin, and alternative diagnoses should be considered. Elevated homocysteine is an independent risk factor for myocardial infarction, stroke, and peripheral arterial atherothrombosis109; it is also an independent risk factor for venous thrombosis, with an odds ratio of approximately 2 to 2. Elevated homocysteine levels can be effectively reduced with folate, vitamin B6, and vitamin B12 supplementation. Surgery and trauma are strong risk factors for the development of venous thrombosis. Myeloproliferative diseases (polycythemia vera, chronic myelogenous leukemia, myeloid metaplasia, essential thrombocytosis), hypergammaglobulinemia, and hyperfibrinogenemia may predispose to thrombosis by causing a hyperviscous state. At clinical presentation, patients manifest cerebral (arterial and venous), coronary, pulmonary and peripheral arterial and venous thromboemboli. Hemolytic-uremic, syndrome and thrombotic thrombocytopenic purpura cause microvascular thromboses and thrombocytopenia. Despite this significant prevalence of thrombophilia, there has been a significant move away from routine testing for several reasons. Thus, the presence or absence of the more common thrombophilias does not significantly affect the recommended duration of anticoagulation in most circumstances. Again, the more common thrombophilias do not factor into the recommended duration of therapy Lastly the risk. Note: A positive thrombophilia evaluation is not a sufficient basis to offer extended anticoagulation. These relatives should receive prophylaxis in high-risk situations regardless of test results. Concomitant administration of oral vitamin K antagonists also decreases protein C and protein S activity If abnormal results are obtained under these conditions, then repeated testing. To avoid the need and expense of repeated testing, many clinicians do not perform the thrombophilia testing until after 3 months of anticoagulation, waiting 2 to 4 weeks after the anticoagulation has been discontinued. Arterial Thromboembolism the relationship between thrombophilia and arterial thrombosis is not as well established. A 2008 large systematic review suggested that several of the heritable and acquired hypercoagulable conditions have a probable association with coronary artery disease, myocardial infarction, and stroke, but there was no identifiable association with peripheral artery disease or thrombosis (Table 6. The available clinical data is unable to provide clear guidance regarding indications for thrombophilia testing in patients with peripheral artery disease and acute arterial thrombosis. In part, this may be due to the complex pathophysiology that results in acute limb or organ ischemia. For example, patients with peripheral artery disease often have multiple other risk factors such as diabetes, hypertension, hyperlipidemia, and tobacco use that contribute to the development of atherosclerosis and atherothrombosis. Many patients with these risk factors will present with acute limb ischemia in the absence of any detectable thrombophilia. Another confounding factor is that patients with acute arterial thromboembolism often have concomitant cardiogenic sources of embolism (atrial fibrillation, aortic or mitral valvular disease, intracardiac thrombus). No significant coronary stenosis on angiography Screen for: Antiphospholipid antibodies Essential thrombocythemia Polycythemia vera Malignancy Cocaine metabolites Homocysteinemia Factor V Leiden Prothrombin 20210 1. We reviewed the prevalence and spectrum of thrombophilia in 112 patients at our institution who presented with acute peripheral artery thrombosis or thromboembolism over a 7-year period, excluding patients with known atherosclerotic occlusive disease and trauma-associated arterial thrombosis. The more common thrombophilias identified in our patients matched those shown in Box 6. Patients with arterial thrombosis and thrombophilia were younger, had fewer comorbidities, and were more likely to have a family history of thrombosis, yet they had a higher rate of limb amputation and mortality when compared with nonthrombophilic patients. Given these results, we test all patients who present with idiopathic peripheral artery thrombosis for antiphospholipid antibodies and myeloproliferative disorders, and make sure they receive age-appropriate screening for malignancy Practically speaking. Now, physicians and patients have several other options available, including orally or intravenously administered direct thrombin inhibitors and orally administered factor Xa inhibitors. The basic pharmacokinetic properties of each of these anticoagulants are shown in Tables 6. Dosing recommendations in risk of accumulation, use approved, risk of package insert. Typically these decisions should be made in collaboration between the vascular surgery and hematology teams. Greater than or equal to one unexplained deaths of a morphologically healthy fetus at or beyond the 10th week gestation 2. Greater than or equal to one premature births of a morphologically healthy newborn before the 34th week of gestation due to eclampsia or severe preeclampsia 3. Greater than or equal to three unexplained consecutive spontaneous abortions before the 10th week of gestation In order to meet laboratory criteria for antiphospholipid syndrome, patients should be test-positive for lupus anticoagulant, anticardiolipin antibodies (IgG or IgM medium or high titers), or anti-2-glycoprotein 1 antibody (IgG or IgM) on at least two occasions (12 weeks apart). Antithrombotic prophylaxis or therapy in this population may be classified as primary (no prior thrombosis) versus secondary (established arterial or venous thrombosis). Primary thromboprophylaxis in patients with systemic lupus and positive lab titers should include hydroxychloroquine and low-dose aspirin. Titer-positive patients without systemic lupus may receive long-term prophylaxis with aspirin alone. Which of the following statements is true regarding perioperative low-molecular-weight heparin bridging Unfractionated heparin and low-molecular-weight heparin have a similar incidence of heparin-associated antibody formation. Thrombophilia testing is indicated for asymptomatic family members of patients with known heritable thrombophilias. A 52-year-old male develops acute left lower extremity ischemia due to superficial femoral artery thrombosis. Which of the following statements regarding the risk associated with pregnancy and hormonal therapy is false The thrombosis risks associated with oral contraceptives are immediate and reversible. Oral contraceptives are associated with a two- to fourfold increased risk for venous thrombosis. Managing new oral anticoagulants in the perioperative and intensive care unit setting. Evidence-based recommendations for the prevention and long-term management of thrombosis in antiphospholipid antibody-positive patients: report of a task force at the 13th International Congress on Antiphospholipid Antibodies. Periprocedural management of patients receiving a vitamin K antagonist or a direct oral anticoagulant requiring an elective procedure or surgery J Thromb Haemost. Update on the relationship of heparin to atherosclerosis and its thrombotic complications. Thrombomodulin, an endothelial anticoagulant protein, is absent from the human brain. Identification of an endothelial cell cofactor for thrombincatalyzed activation of protein C. Distribution of tissue factor pathway inhibitor in normal and malignant human tissues. Cultured normal human hepatocytes do not synthesize lipoprotein-associated coagulation inhibitor: evidence that endothelium is the principal site of its synthesis. Platelets secrete a coagulation inhibitor functionally and antigenically similar to the lipoprotein associated coagulation inhibitor. The extrinsic pathway inhibitor: a regulator of tissue factordependent blood coagulation. A steady-state template model that describes the kinetics of fibrin-stimulated [Glu1] and [Lys78] plasminogen activation by native tissue-type plasminogen activator and variants that lack either the finger or kringle-2 domain. Prophylactic platelet administration during massive transfusion: a prospective, randomized, doubleblind clinical study Ann Surg. A revised classification of von Willebrand disease: for the Subcommittee on von Willebrand Factor of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis. Bleeding diathesis due to decreased functional activity of type 1 plasminogen activator inhibitor. National estimates of emergency department visits for hemorrhage-related adverse events from clopidogrel plus aspirin and from warfarin. Trial of different intensities of anticoagulation in patients with prosthetic heart valves. Increased risk of intracranial hemorrhage when aspirin is combined with warfarin: a meta-analysis and hypothesis. Warfarin plus aspirin after myocardial infarction or the acute coronary syndrome: meta-analysis with estimates of risk and benefit. New strategies for effective treatment of vitamin K antagonistassociated bleeding. Emergency oral anticoagulant reversal: the relative efficacy of infusion of fresh frozen plasma and clotting factor concentrate on correction of the coagulopathy Thromb Haemost. Periprocedural heparin bridging in patients receiving vitamin K antagonists: Systematic review and meta-analysis of bleeding and thromboembolic rates. Venous thrombosis due to poor anticoagulant response to activated protein C: Leiden Thrombophilia Study. High risk of thrombosis in patients homozygous for factor V Leiden (activated protein C resistance). Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men. Factor V Cambridge: a new mutation (Arg306Thr) associated with resistance to activated protein C. A factor V genetic component differing from factor V R506Q contributes to the activated protein C resistance phenotype. A common genetic variation in the 3untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. The risk of recurrent deep venous thrombosis among heterozygous carriers of both factor V Leiden and the G20210A prothrombin mutation. Treatment of venous thromboembolism in patients with congenital deficiency of antithrombin. Absence of thrombosis in subjects with heterozygous protein C deficiency N Engl J Med. Protein C deficiency in a controlled series of unselected outpatients: an infrequent but clear risk factor for venous thrombosis (Leiden Thrombophilia Study).

The incidence and risk factors of cholesterol embolization syndrome planetary herbals quality discount 30caps himplasia fast delivery, a complication of cardiac catheterization: a prospective study herbals and glucocorticoids buy cheap himplasia on-line. Peripheral vascular complications of coronary angioplasty by the femoral and brachial techniques zever herbals purchase himplasia 30caps online. Scraping of aortic debris by coronary guiding catheters: a prospective evaluation of 1 herbs to grow indoors buy himplasia cheap online,000 cases herbals on deck himplasia 30caps otc. Risk of catheter-related emboli in patients with atherosclerotic debris in the thoracic aorta baikal herbals 30caps himplasia visa. Warfarin safety and efficacy in patients with thoracic aortic plaque and atrial fibrillation. Atherosclerotic disease of the aortic arch as a risk factor for recurrent ischemic stroke. Cholesterol crystal embolization-associated renal failure after therapy with recombinant tissue-type plasminogen activator. Acute renal failure after streptokinase therapy in a patient with acute myocardial infarction. Cholesterol embolization syndrome after intravenous tissue plasminogen activator for acute myocardial infarction. Prospective assessment of cholesterol embolization in patients with acute myocardial infarction treated with thrombolytic vs. Livedo reticularis: an underutilized diagnostic clue in cholesterol embolization syndrome. Cholesterol crystal embolization to the digestive system: characterization of a common, yet overlooked presentation of atheroembolism. Focal segmental glomerulosclerosis associated with nephrotic syndrome in cholesterol atheroembolism: clinicopathological correlations. The characteristics of dissemination of embolic materials during renal artery stenting. Etiologies and outcome of acute renal insufficiency in older adults: a renal biopsy study of 259 cases. Reversible nephrotic range proteinuria and renal failure in atheroembolic renal disease. Supportive treatment improves survival in multivisceral cholesterol crystal embolism. Case report: atheroembolic renal disease in a 72-year-old patient through coronary intervention after myocardial infarction. Predictors of renal and patient outcomes in atheroembolic renal disease: a prospective study. Multiple spontaneous small bowel perforations due to systemic cholesterol atheromatous embolism. Atheromatous embolization resulting in acute pancreatitis after cardiac catheterization and angiographic studies. Ischemic colitis and acalculous necrotizing cholecystitis as rare manifestations of cholesterol emboli in the same patient. Atheromatous embolization to the stomach: an unusual cause of gastrointestinal bleeding. Early experience using the Wallgraft in the management of distal microembolism from common iliac artery pathology. Mobile thrombi in the abdominal aorta in cases of lower extremity embolic arterial occlusion: value of extended transthoracic echocardiography. The role of aortic stent grafting in the treatment of atheromatous embolization syndrome: results after a mean of 15 months follow-up. The role of extraanatomic exclusion bypass in the treatment of disseminated atheroembolism syndrome. Blue toe syndrome: treatment with anticoagulants and delayed percutaneous transluminal angioplasty. Filters placed in the superficial femoral arteries for limb salvage in a high-surgical-risk patient with atheroembolism: results at 2 years. Value of transoesophageal echocardiography for the diagnosis of embolic lesions from the thoracic aorta. A transesophageal echocardiographic finding associated with unexplained arterial embolism. Aortic plaque morphology and vascular events: a follow-up study in patients with ischemic stroke. Mild to moderate atheromatous disease of the thoracic aorta and new ischemic brain lesions after conventional coronary artery bypass graft surgery. Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography. Protruding atherosclerotic plaque in the aortic arch of patients with systemic embolization: a new finding seen by transesophageal echocardiography. Atherosclerosis of the thoracic aorta and aortic debris as a marker of poor prognosis: benefit of oral anticoagulants. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies. Mobile aortic atheroma and systemic emboli: efficacy of anticoagulation and influence of plaque morphology on recurrent stroke. The significance of microemboli detection by means of transcranial Doppler ultrasonography monitoring in carotid endarterectomy. Clinical characteristics of pathologically proved cholesterol emboli to the brain. Protected carotid stenting: clinical advantages and complications of embolic protection devices in 442 consecutive patients. Benefits of cerebral protection during carotid stenting with the PercuSurge GuardWire system: midterm results. Effect of treatment on the incidence of stroke and other emboli in 519 patients with severe thoracic aortic plaque. Pain relief and clinical improvement temporally related to the use of pentoxifylline in a patient with documented cholesterol emboli-a case report. Low-density lipoprotein apheresis ameliorates renal prognosis of cholesterol crystal embolism. Creager Abstract Raynaud phenomenon is a common episodic vasospastic disorder, brought on by cold exposure or stress, and relieved by rewarming. It can be classified as either primary (idiopathic) or secondary (associated with another disease process). Detailed history, physical examination, and focused laboratory evaluation are key to differentiating primary versus secondary Raynaud phenomenon. Although the pathophysiology is not fully understood, it is likely that multiple factors play a role, including local vascular hyperreactivity, increased sympathetic nervous system activity, elevated levels of vasoconstrictor hormones, and exogenous agents. Treatment is individualized; conservative measure of avoiding unnecessary cold exposure is the mainstay. Digital sympathectomy can be considered in refractory cases of secondary Raynaud phenomenon with threatened tissue loss. Keywords Raynaud phenomenon; vasospasm; vasoconstriction; vascular hyperreactivity; collagen vascular diseases In its simplest form, local syncope is a condition perfectly compatible with health. Under the least stimulus, sometimes without appreciable cause, one or many fingers become pale and cold all at once; in many cases, it is the same finger that is always first attacked; the others become dead successively and in the same order. The determining cause is often the impression of cold; but that which is only commonly produced under the influence of the most severe cold, appears in the subjects of whom I speak on the occasion of the least lowering of temperatures; sometimes even a simple mental emotion is enough. The cutaneous sensibility becomes blunted, then annihilated; the fingers become like foreign bodies to the subject. This patch gives place to the normal pink colour, and then the skin is found to have entirely returned to the primitive condition. The color changes are usually well demarcated and primarily confined to fingers or toes. Blanching, or pallor, occurs during the ischemic phase of the phenomenon and is secondary to digital vasospasm. Cold, numbness, or paresthesias of the digits often accompany the phases of pallor and cyanosis. With rewarming, digital vasospasm resolves, and blood flow dramatically increases into the dilated arterioles and capillaries. In addition to rubor and warmth, patients often experience a throbbing sensation during the hyperemic phase. Although the triphasic color response is typical of Raynaud phenomenon, some patients may develop only pallor and cyanosis. Secondary causes of Raynaud phenomenon include collagen vascular diseases, arterial occlusive disease, thoracic outlet syndrome, several neurological disorders, blood dyscrasias, trauma, and several drugs or toxins. Primary Raynaud phenomenon is common and may affect up to 8% of the general population in the United States;5 women are significantly more affected than men. Onset usually occurs before the fourth decade of life, with higher prevalence in cooler climates. Raynaud phenomenon is also known to occur in children, more often in girls than boys, and prevalence increases in age. Later, color changes may develop in additional fingers, and symptoms occur bilaterally. In about 40% of patients, Raynaud phenomenon involves the toes as well as the fingers. Episodes of Raynaud phenomenon are usually precipitated by exposure to a cool environment or by direct exposure of the extremities to low temperatures. Some patients may experience Raynaud phenomenon during either cold exposure or emotional stress; infrequently, emotional stress may be the only precipitating factor. Duration, frequency, and severity of Raynaud phenomenon increase during cold months. Multiple studies have correlated Raynaud phenomenon with vasospastic disorders, including migraine headaches,9 variant angina,10,11 and vasospasm in the kidney,12 retina,13 and pulmonary vessels. For example, metoprolol and propranolol have been successfully used to prevent migraines headaches,15 but are not beneficial in variant angina and may precipitate Raynaud phenomenon. The pulse examination is normal; radial, ulnar, and pedal pulses should be easily palpable. Trophic changes such as sclerodactyly (thickening and tightening of the digital subcutaneous tissue) occur in less than 10% of patients. The physical examination is most important to exclude secondary causes of Raynaud phenomenon. Of all the forms of Raynaud phenomenon, primary Raynaud phenomenon has the most benign prognosis. In a historical group of patients identified by Gifford and Hines20 followed for a period of 1 to 32 years (average 12 years), 16% reported worsening of their symptoms, and 38%, 36%, and 10%, respectively, reported no change, improvement, or disappearance of symptoms. Sclerodactyly or trophic changes of the digits occurred in approximately 3% of patients during follow-up, and less than 1% of patients lost part of a digit. Scleroderma pattern on nailfold capillaroscopy was the most sensitive marker of scleroderma development, while absence of anti-topoisomerase I antibodies was the most specific. It is quite likely that a variety of physiological and pathological conditions may contribute to or cause digital vasospasm (Box 46. Digital vasospasm may be due to vasoconstrictive stimuli, decreased intravascular pressure, or both. Mechanisms that contribute to exercise vasoconstriction include local vascular hypersensitivity to vasoactive stimuli. Low blood pressure, even in a healthy young person, may predispose to Raynaud phenomenon when the person encounters vasoconstrictive stimuli. Pathological conditions that may decrease intravascular pressure include arterial occlusion in proximal arteries. Normally, regulation of peripheral blood flow depends on several factors that include intrinsic vascular tone, sympathetic nervous system activity, hemorrheological properties such as blood viscosity, and various circulating hormonal substances. In contrast to other regional circulations that are supplied by both vasoconstrictor and vasodilator sympathetic fibers, the cutaneous vessels of the hands and feet are innervated only by sympathetic adrenergic vasoconstrictor fibers. In these vascular beds, neurogenic vasodilation occurs by withdrawal of a sympathetic stimulus. Cooling evokes reflex sympathetic-mediated vasoconstriction in the hands and feet via neurons originating in cutaneous receptors. Environmental cooling or cooling of specific body parts, such as the head, neck, or trunk, also causes a reduction in digital blood flow. Local digital cooling also induces vasoconstriction, independent of increased sympathetic tone. Raynaud phenomenon is not a normal physiological response but rather an episode of digital artery vasospasm causing decrease of blood flow to the digits. Vasoconstriction may be defined as the expected reduction in vessel lumen size as a result of endogenous neural, hormonal, or metabolic factors that cause smooth muscle contraction. Vasospasm implies an excessive vasoconstrictor response to stimuli that would normally cause modest smooth muscle contraction, but that instead has resulted in obliteration of the vascular lumen. Patency of the digital artery depends on a favorable balance between the contractile forces of the muscular wall of the digital artery and its intraluminal pressure. Thus, a situation in which there is excessive vasoconstrictive force or decreased intravascular pressure upsets this balance and results in vasospasm. It is with these rather simple concepts that several theories have been proposed to explain the episodic digital vasospasm that defines Raynaud phenomenon. Increased Vasoconstrictive Stimuli Several theories implicate excessive vasoconstrictive stimuli as a cause of Raynaud phenomenon. Postulated causes include local vascular hyperreactivity, increased sympathetic nervous system activity, elevated levels of vasoconstrictor hormones. Local Vascular Hyperreactivity the observation that episodic digital vasospasm occurs during cold exposure has led several investigators to consider the possibility that Raynaud phenomenon occurs as a result of a local vascular hyperreactivity.

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