Ajmal Masood Gilani, MD

• Neurologist
• Johnson Neurology
• Clayton, North Carolina

This observation was subse quently validated in patients undergoing operation with general anesthesia acne and pregnancy order elimite no prescription. This method is sensitive acne and dairy cheap elimite 30gm with mastercard, easy to use acne queloide discount elimite 30 gm online, and has the advan tage of providing continuous monitoring rather than a single 417 or residual stenosis skin care untuk kulit berjerawat order elimite from india. A transverse arteriotomy is made just distal to the residual lesion acne under microscope cheap elimite 30gm without a prescription, and the remaining plaque is removed skin care zo elimite 30gm with amex. The transverse arteriotomy is closed with inter rupted polypropylene sutures, and flow is restored. Closure consists of a running absorb able suture in the platysma layer and a running absorbable subcuticular suture for cosmetic skin closure. Irrigating the wound with a dilute antibiotic solution and observing for bleeding sites ( to be controlled with ligature or electrocoagulation) may be the best strategy. A deep wound infection may affect a 33 prosthetic patch and threaten the integrity of the carotid artery. If no neurological deficits are noted,the patient is transferred to the recovery room for monitoring. Once the patient is fully awake, the blood pressure controlled, and the neck free of hematoma, the patient is transferred to a regular hospital room for overnight observation. Regulation of blood flow is impaired on the side of endarterectomy for approximately 3 to 6 weeks, so the ipsilateral cerebral hemisphere is vulnerable to elevated postoperative blood pressure. Uncontrolled hyperten sion can result in excessive perfusion pressure, the consequences of which range from headache to seizures and lead to intracere bral bleeding resulting in major stroke or death. Hypotension and bradycardia occur from baroreceptor activation caused by stimu lation of the nerve to the carotid sinus. If the patient is stable overnight and does not have a new neurological complication, he or she can be discharged the following morning. The patient is instructed to resume usual medi cations, including an antiplatelet agent. The first postoperative visit should occur in approximately 3 weeks, at which time a carotid duplex ultrasound scan is per formed to assess the result of endarterectomy and establish a new baseline for further followup. Additional carotid ultrasound examinations are recommended at 6 months and then 1 year from the time of operation. The trial was divided in to two cohorts; one involved patients with carotid artery stenosis of 70% to 99%, and the other involved patients with stenosis of 50% to 69%. It was stopped after 189 patients were entered as the results of the North American and European trials were reported. Patients with expanding hematomas should return to the operating room for evacuation and restitution of hemostasis. Judicious use of heparin, particularly if the patient is on more than one antiplatelet agent, is important. Carotid Endarterectomy Compared to Carotid Angioplasty/Stenting Carotid artery angiography and stenting is described in detail in Chapter 32. These differences persisted for 1 year, but by 4 years, there was no difference between the two groups regarding eventfree survival. The study patients were followed for 4 years, at which time the death and stroke rates were 6. Twelve hundred patients were randomized, but the study was stopped because a futility analysis was performed indicating that the pri mary hypothesis could not be proved. It involved 50 academic centers in the United Kingdom, Europe, Australia, New Zealand, and Canada. Between the years 2000 and 2008, 2502 patients were randomized; 47% were asymptomatic, and 53% were symptomatic. The initial analysis occurred after the last group of patients had at least 1 year of followup, and median follow up was 2. Carrea R, Molins M, Murphy G: Surgical treatment of spontaneous thrombosis of the internal carotid artery in the neck: carotid-carotidal anastomosis. Gowers W: On a case of simultaneous embolism of central retinal and middle cerebral arteries, Lancet 2:794, 1875. The terms communicating and noncommunicating refer to the presence or absence, respectively, of blood flow between the true and false lumens of the aorta. Aortic dissection is acute if presentation occurs within 14 days of the onset of symptoms and chronic if more than 2 weeks have elapsed. Morbidity and mortality are highest within the acute phase; patients who have survived without treatment for 2 weeks are self-selected for better short- and intermediate-term outcomes. In practice, diagnosis of aortic dissection depends on demonstration with imaging of an intimal flap with separation of true and false lumens. In type A dissection, the true lumen is usually displaced along the inner curvature of the aortic arch and continues caudally along the medial aspect of the descending thoracic aorta. Aortic branch vessel blood flow may derive from either the true or false lumen; alternatively, flow may be sluggish or absent within the false lumen, or branch vessels may be completely occluded at or near their origins. Acute aortic dissection is an uncommon but life-threatening emergency that requires prompt diagnosis, rapid triage, and immediate medical, endovascular, or surgical treatment. A unified effort across several international centers over the past 15 years has led to the establishment of a detailed registry that describes major aspects of presentation, management, and outcomes of patients with acute aortic dissection. Although gains have been made in the delivery of life-saving care to patients with acute aortic dissection, hospital mortality rates remain distressingly high. Enhanced awareness of risk factors for aortic dissection, presentation features, diagnostic pathways, and medical, endovascular, and surgical treatment strategies is a critical first step toward improving outcomes. Epidemiology Published figures on the incidence of aortic dissection likely underestimate the actual occurrence rate, since misdiagnosis of this condition is common and the percentage of acute aortic dissection patients who expire before hospital presentation cannot be accurately estimated. Analysis of the Swedish National Cause of Death Register between 1987 and 2002 estimated the incidence of thoracic aortic aneurysm or dissection to be 16. In classic acute aortic dissection, the initiating event is an intimal tear through which blood rapidly surges distally in to the media under systolic pressure, splitting the layers of the aortic wall and creating an intimal flap that separates the true from the false lumen. Classification Classifying aortic dissection according to anatomical location and time from onset of symptoms helps stratify risk and guide selection of initial treatment strategy. The Stanford classification system designates dissections that involve the aorta proximal to the brachiocephalic artery. In the older DeBakey classification scheme, a type I dissection originates within the ascending aorta and extends for a variable distance beyond the take-off the innominate artery. It is most frequently located a few centimeters above the level of the aortic valve along the greater curvature of the aorta in cases of type A dissection and accounts for nearly 60% of all cases. Compared with other locations in the ascending aorta, the proximal few centimeters of the greater curvature are exposed to relatively greater hemodynamic, shear, and torsional force. By this mechanism, as many as 20% of dissections that originate in the distal arch or descending thoracic aorta may involve the ascending aorta. Blood within the false lumen may reenter the true lumen anywhere along the length of the dissection. Reentry may be protective because of spontaneous decompression of the false lumen that may reduce the risks of rupture and/or development of malperfusion syndromes. Acquired Aortic Rupture and End-Organ Malperfusion Aortic rupture, defined as tearing in the vessel wall that results in extravascular hemorrhage, most commonly occurs with trauma. Dissection-mediated end-organ ischemia or infarction occurs from (1) mechanical compression of aortic branch vessels by false lumen hematoma, (2) extension of the dissection plane across the ostium of the branch vessel, or (3) dynamic vessel inlet obstruction caused by an oscillating intimal flap. The abdominal aorta is the least common site for entry (3% of cases), despite the high prevalence of intima media ulcers in patients with atherosclerotic disease in this segment. A, Computed tomographic image demonstrates three-channel descending aortic dissection in Marfan syndrome patient. B, Schematic representation of dissection is provided: region 1 represents thrombosed false lumen, region 2 is true lumen significantly diminished in size, and region 3 designates contrast-enhanced false lumen. False Lumen Thrombosis Thrombosis of blood within the false lumen may seal the entry tear, thus eliminating communication with the true lumen and interruption of false lumen expansion. Partial thrombosis of the false lumen, however, has been identified as a risk factor for long-term death in patients with type B dissection. Alternatively, it has been proposed that partial thrombosis of the false lumen is associated with worse clinical outcomes by promoting vascular inflammation, hypoxia, and/or neovascularization with weakening of adjacent vascular structures and an increased risk for aortic rupture. A, Hematoxylin and eosin microscopic section of aorta reveals fragmentation and loss of elastin fibers with cyst-like structures present within media. This phenotype is felt to be associated with aortic wall weakening and increased predisposition to dissection. Deceleration injury from high-speed accidents results in aortic transection with false aneurysm formation and rupture, most commonly in the region of the aortic isthmus just beyond the origin of the left subclavian artery. In many cases, pregnancy unmasks primary conditions that predispose to aortic dissection. Decreased aortic compliance and vulnerability to pulsatile forces predispose to injury and create a substrate for dissection. Drug Use and Other Acquired Conditions Recent cocaine use, particularly among young men who smoke tobacco, is an additional risk factor for aortic dissection. Chronic amphetamine use and/or dependence appear to increase the probability of developing a thoracoabdominal aortic dissection in those aged 18 to 49 years. Retrograde dissections created at the time of catheterization usually seal spontaneously on withdrawal of the catheter. Aortic atherosclerotic plaques may prevent longitudinal propagation of a dissection. Pheochromocytoma and weight lifting (believed due to intense or repetitious Valsalva maneuvers) also predispose to aortic dissection. Absent an appreciation for the cardinal features of dissection, the diagnosis can be missed in a substantial number of patients. Simple clinical prediction rules have been developed to estimate probability of acute aortic dissection. These markers, assessed at bedside, were divided in to three distinct categories: predisposing factors, characteristics of the pain at time of presentation, and key physical examination findings. Visceral discomfort or limb pain may be indicative of aortic branch vessel ischemia from malperfusion. Syncope is a particularly ominous presenting symptom and may reflect cardiac tamponade from intrapericardial aortic rupture, cerebral malperfusion, and/or neurally mediated hypotension in response to the intense pain of the dissection. For example, paraplegia may develop when critical impairment of flow to the anterior spinal artery, thoracic intercostals, or the artery of Adamkiewicz occurs. Abdominal pain is an underrecognized symptom of acute aortic dissection; when present, it is associated with elevated in-hospital mortality and increased frequency of malperfusion syndromes. A retrospective analysis of the International Registry of Acute Aortic Dissection determined that among 2538 patients with acute aortic dissection, 95. Hypertension is present in more than two thirds of type B dissection patients and in approximately one third of type A patients. Additional auscultatory findings include a soft first heart sound and a grade 1 or 2 midsystolic murmur at the base or along the left sternal border. An inverse correlation between the presence of pulse deficits and mortality is observed in acute aortic dissection. Thus, invasive intraarterial monitoring may be necessary in aortic dissection patients. Elevation of jugular venous pressure, especially with pulsus paradoxus, may indicate pericardial involvement with tamponade. Superior vena cava syndrome can rarely occur with compression by an expanding false aneurysm along the greater curvature of the ascending aorta. In fact, pleural effusions are quite frequent with both type A and B dissections; they are usually sympathetic in nature, reflective of the intense inflammation associated with the acute tear. Sensitivity and specificity of these three noninvasive techniques are essentially equivalent and exceed 90% in most series. Regardless of the diag- 34 nostic sequence employed, an institutional commitment to rapid imaging of critically ill patients is critical. Essential features to be defined for both treatment and prognosis include presence or absence of ascending aortic involvement, entry and reentry sites, pericardial and aortic valve involvement, extent of the dissection, major branch vessel compromise, and the anatomical substrate for potential malperfusion syndrome(s). Oropharyngeal anesthesia and conscious sedation are required, with simultaneous monitoring of heart rate and rhythm, blood pressure, and oxygen saturation. In most cases, the true lumen is differentiated from the false lumen by observing systolic expansion and diastolic collapse, absence or minimal spontaneous echo contrast, and/or an antegrade Doppler signal. In one study of 95 patients with acute aortic dissection, elevated levels of circulating smooth muscle myosin heavy chain protein (>2. Consistent with these data, findings from one large meta-analysis of 734 patients demonstrated that an elevated D-dimer level had a 97% sensitivity and 96% negative predictive value for identifying acute aortic dissection. Conversely, an elevated D-dimer is less effective at "ruling-in" aortic dissection, with a specificity of 56% and positive predictive value of 60%. Associated findings may include cardiomegaly (pericardial effusion) and pleural effusion (left > right). Effusions that occupy more than 50% of the chest cavity may be indicative of rupture with hemothorax. Additional findings include displacement of intimal calcium, delayed contrast enhancement of the false lumen, and aortic widening. Branch vessel involvement anywhere along the course of the aorta to the level of the iliac arteries can be precisely displayed.

Intravascular ultrasound may also have a role during performance of endovascular procedures acne 6dpo purchase elimite 30gm. Systematic preoperative coronary angiography for hemodynamically stable chronic type A dissection patients is a subject of debate skin care websites purchase elimite in united states online. Identification of high-grade atherosclerotic disease of native coronary arteries and/or coronary artery bypass graft(s) affords determination of the optimal operation for patients requiring ascending aortic surgery skin care with ross buy elimite now. However skin care equipment buy generic elimite, in these instances skin care 29 year old elimite 30gm line, the potential for incorporating additional surgical procedures beyond repairing the dissection should be evaluated on a case-by-case basis acne juice cleanse order elimite 30 gm without a prescription. Surgery or endovascular stent grafting when feasible can be undertaken for failed medical therapy, pseudoaneurysm, or rupture. Differential Diagnosis Other Acute Aortic Syndromes Aortic transection from deceleration injury and traumatic aortic valve disruption with acute severe aortic regurgitation occur in the setting of high-speed vehicular accidents or vertical falls. The nontraumatic acute aortic syndromes, however, are often not distinguishable from classic dissection on clinical grounds alone, but rather are delineated with cross-sectional imaging. Predicting evolution to dissection, rupture, aneurysm formation, or false aneurysm development is difficult. Imaging studies in the former disease states may reveal wall thickening and periaortic stranding or hematoma, as well as a measurable increase in aortic dimensions when compared with available past studies. Rapid expansion of the Marfan aorta occurs for reasons not related to inflammation, but when present may be even more worrisome. Esmolol Propranolol 1 (9 min) 1 2 (5-7 h) Initial Medical Treatment Patients with acute aortic syndromes should be treated with intravenous medications to lower the arterial blood pressure as expeditiously as possible. Target systolic blood pressure and heart rate are 110 mmHg and 60 beats/min or less, respectively, but medications may require titration according to clinical evidence of impaired end-organ perfusion. In Step 1, a low index of clinical suspicion for acute aortic dissection should prompt early diagnostic testing while medical therapy is initiated. Step 2 involves determination of ascending aortic involvement, which significantly influences importance of emergent surgical consultation. In Step 3, patients with type A aortic dissection are referred for surgery, and patients with complicated type B aortic dissection are referred for endovascular therapy or surgery. Patients with uncomplicated type B aortic dissection are continued on medical therapy and monitored for changes in clinical status. In Step 4, a care plan is established that emphasizes importance of long-term medical therapy, radiological surveillance, and lifestyle modifications to decrease risk of postdissection complications. The starting dose is 25 g/min by continuous infusion, and adjustments are usually made in increments of 10 to 25 g. Alternative intravenous vasodilators available for use in the acute setting include enalaprilat, hydralazine, and nicardipine. For acute aortic dissection patients with hypotension, cardiogenic shock from hemopericardium should be considered. Volume resuscitation or pressor therapy may be necessary to maintain vital organ perfusion, but these are merely temporizing measures. Pericardiocentesis for relief of tamponade is not recommended, and surgery should be performed emergently. The extent and complexity of surgery (resection/grafting of the ascending aorta, valve resuspension or replacement, coronary artery reimplantation) is determined on a case-by-case basis. Incorporation of the aortic arch in the primary repair is indicated when the tear traverses this segment of the aorta or when it has become acutely aneurysmal. In this situation, surgeon preference and patient comorbidities weigh heavily in decision making, as does any information related to aortic enlargement over time. Outcomes with conservative management may not be inferior to surgical repair in the chronic phase, as suggested by limited single center experiences and retrospective data. There is evolving evidence to support a relationship between clinical outcome and operator experience in repair of aortic disease. Increasing hospital volume for open abdominal aortic aneurysm repair is associated with improved survival, particularly at centers that perform over 50 abdominal aortic aneurysm repairs annually. Ongoing public health initiatives have proposed examining the following variables to define centers of excellence for surgical repair of thoracic aortic disease: procedural volumes (operator and facility), outcome, time to Type B Aortic Dissection Uncomplicated type B dissection is treated medically, with emphasis on tight heart rate and blood pressure control. Lifestyle modifications, including the possibility of career change, may be necessary to avoid strenuous lifting, pushing, or straining that requires intense or repetitive Valsalva maneuvers. The importance of refractory pain in otherwise uncomplicated type B dissection is increasingly appreciated. In one recently published prospective analysis of 365 type B dissection patients without conventional high-risk features, the presence of pain or persistent hypertension despite medical therapy was associated with a 35-fold increase in mortality, compared with the absence of these clinical features. Several nonrandomized small prospective trials and registries have shown that endovascular stent grafting for acute, subacute, or chronic type B dissection can be an effective lowerrisk alternative to surgery. Most high-volume centers have moved in this direction, and it is unlikely that a pivotal trial versus surgery will be conducted in patients with traditional indications for surgery in type B dissection. Independent predictors of early mortality include advanced age, rupture, and malperfusion syndromes. The excess mortality risk imposed by early complications necessitating surgical treatment,and thus operation on acutely sicker patients,has prompted investigation of endovascular stent grafting for selected patients. Nearly 2 decades of experience with thoracic endovascular aortic repair have yielded encouraging results regarding short- and long-term efficacy rates for this treatment strategy. One retrospective analysis of 87 patients undergoing endovascular stent placement to treat acute type B dissection demonstrated a 30-day survival rate of 81%, despite the presence of hemodynamic instability or shock in 62% of the study population. Complete or partial false lumen patency or maximal descending thoracic aortic diameter of 4. These data are concordant with others suggesting positive aortic remodeling in type B dissection patients following endovascular stent graft placement. It is unclear whether positive aortic remodeling will impact clinical outcomes longer term. Endoleak, stroke, and other device complications including migration and thrombosis have been reported. In this procedure, a balloon catheter is used to create a transverse tear across the dissection flap to attenuate compressive forces on the true lumen and improve flow to compromised organs. Medical management remains targeted to strict blood pressure (130/80 mmHg) and heart rate (60 beats/min) goals. Strenuous exercise is discouraged, and patients need be educated regarding the chronic nature of this disease, self-awareness of dissection-associated symptoms, and the importance of medication adherence. Imaging of the entire aorta is recommended pre-discharge and at 1, 3, 6, and 12 months, then annually thereafter. Increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14,000 cases from 1987 to 2002, Circulation 114:2611, 2006. Eggebrecht H, Baumgart D, Schmermund A, et al: Penetrating atherosclerotic ulcer of the aorta: treatment by endovascular stent-graft placement, Curr Opin Cardiol 18:431, 2003. Ando M, Okita Y, Tangusari O, et al: Surgery in three-channeled aortic dissection. Richen D, Kotidis K, Neale M, et al: Rupture of the aorta following road traffic accidents in the United Kingdom 1992-199. The results of the co-operative crash injury study, Eur J Cardiothorac Surg 23:143, 2003. Kazi M, Thyberg J, Religa P, et al: Influence of intraluminal thrombus on structural and cellular composition of abdominal aortic aneurysm wall, J Vasc Surg 38:1283, 2003. Gary T, Seinost G, Hafner F, et al: Cystic medial necrosis Erdheim Gsell as a rare reason for spontaneous rupture of the ascending aorta, Vasa 40:147, 2011. Ketenci B, Enc Y, Ozay B, et al: Perioperative type I aortic dissection during conventional coronary artery bypass surgery: risk factors and management, Heart Surg Forum 11:E231, 2008. Suzuki T, Katoh H, Tsuchio Y, et al: Diagnostic implications of elevated levels of smoothmuscle myosin heavy-chain protein in acute aortic dissection. Shinohara T, Suzuki K, Okada M, et al: Soluble elastin fragments in serum are elevated in acute aortic dissection, Atherioscler Thromb Vasc Biol 23:1839, 2003. Schillinger M, Domanovits H, Bayegan K, et al: C-reactive protein and mortality in patients with acute aortic disease, Intensive Care Med 28:740, 2002. Erbel R, Alfonso F, Boileau C, et al: Diagnosis and management of aortic dissection: recommendations of the task force on aortic dissection, European Society of Cardiology, Eur Heart J 22:1642, 2001. Bossone E, Evangelista A, Isselbacher E, et al: Prognostic role of transesophageal echocardiography in acute type A aortic dissection, Am Heart J 253:1013, 2007. Hayashi H, Matsuoka Y, Sakamo to I, et al: Penetrating atherosclerotic ulcer of the aorta: imaging features and disease concept, Radiographics 20:995, 2000. Motallebzadeh R, Batas D, Valencia O, et al: the role of coronary angiography in acute type A dissection, Eur J Cardiothorac Surg 25:231, 2004. Motoyoshi N, Moizumi Y, Komatsu T, et al: Intramural hematoma and dissection involving ascending aorta: the clinical features and prognosis, Eur J Cardiothorac Surg 24:237, 2003. Ganaha F, Miller C, Sugimo to K, et al: Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer, Circulation 106:342, 2002. Singhai P, Lin Z: Penetrating atheromatous ulcer of ascending aorta: a case report and review of the literature, Heart Lung Circ 17:380, 2008. The empirical relation between surgical volume and mortality, Clin Orthop Relat Res 457:3, 2007. Sun L, Qi R, Zhu J, et al: Total arch replacement combined with stented elephant trunk implantation: a new "standard" therapy for type A dissection involving repair of the aortic arch, Circulation 123:971, 2011. Yanagisawa S, Yuasa T, Suzuki N, et al: Comparison of medically versus surgically treated acute type A aortic dissection in patients <80 years old versus >80 years old, Am J Cardiol 108:453, 2011. In recent literature, operative mortalities of nearly 50% have been reported for octogenarian patients. Surgical results of institutions and communities have to be considered to optimize best outcomes. In patients whose limited physiological reserve makes them poor candidates for emergency aortic repair, delayed management with initial medical optimization followed by elective surgery may be a reasonable alternative. In most cases of mild to moderate malperfusion, surgical repair of the proximal aorta redirects flow in to the true lumen and restores adequate peripheral blood flow; however, patients in whom ischemia has caused severe end-organ dysfunction are unlikely to benefit from immediate ascending aortic repair. On the basis of these results, these surgeons initiated a policy of delayed surgical treatment in patients with severe malperfusion. Of the 20 patients treated with this strategy, 17 underwent delayed operation an average of 20 days after presentation. The overall survival for these patients treated without immediate operation (15/20, 75%) was significantly better than the dismal survival obtained with a strategy of immediate surgery. Presence of prosthetic aortic valves, aortic suture lines, coronary the treatment of aortic dissections remains technically challenging to surgeons. Patients can present with a wide range of anatomical and physiological derangements. Surgical decisions are made on the basis of three primary considerations: anatomical location of the dissection, time since the onset of dissection, and resulting complications of dissection. The DeBakey and Stanford classifications define dissections according to their anatomical location; both systems place great importance on the involvement of the ascending aorta1. DeBakey type I dissection initiates in the ascending aorta and extends varying distances in to the thoracoabdominal aorta, often reaching the aortic bifurcation. Timing of the operation is important because surgical repair becomes safer as the dissection becomes older and the aorta less fragile. Risks posed by tissue fragility must be weighed against the competing risk of acute complications, which include rupture, heart failure, and malperfusion. Although arbitrary, dissection is considered acute within the first 14 days after the initial tear in the aortic wall. Additionally, aortic dissections can produce a wide variety of lifethreatening complications that may mandate emergent surgical repair or correction. In subsequent aortic segments, malperfusion of branch vessels can cause stroke, paraplegia, mesenteric ischemia, renal failure, and limb-threatening ischemia. The potential for these acute complications, combined with severe physiological derangement and extreme tissue fragility, make aortic dissection one of the most challenging conditions faced by cardiovascular surgeons. These considerations are the foundations of operative indications and strategies for aortic dissection. Surgical strategies for treating proximal aortic dissections involving the ascending aorta and transverse aortic arch differ distinctly from strategies for treating distal aortic dissections involving the descending thoracic and thoracoabdominal aorta; therefore, the proximal and distal aortic segments will be discussed independently. Acute Proximal Dissection Without treatment, nearly half of patients with acute proximal aortic dissection die within 48 hours. Indications for Operation Proximal aortic repairs performed in the chronic phase uniformly have better outcomes than those performed in the acute phase. Unfortunately, the high risk associated with early operation is outweighed by the even higher risk of a fatal complication. Therefore, the presence of an acute proximal aortic dissection has traditionally been considered an absolute indication for emergency surgical repair. The primary limitation of the Stanford classification is that it is based solely on presence (type A) or absence (type B) of ascending aortic involvement; it does not provide information about distal aortic involvement, a factor that has important management and prognostic implications. Weakened aortic wall can rupture at any location and often results in fatal exsanguination. Aortic dissection can lead to acute cardiac failure via (B) extension in to coronary ostia, causing myocardial ischemia, and (C) disruption of aortic valve commissures, causing valvular insufficiency. Complications of branch vessel malperfusion include (D) stroke or upper-extremity ischemia when brachiocephalic branches are involved, paraplegia when segmental intercostal and lumbar arteries are compromised, (E) renal failure or mesenteric ischemia when visceral vessels are disrupted, and (F) lower-limb ischemia when iliac arteries are occluded. Implementation of the protocol developed by the Stanford Health Care Life Flight program decreased the number of patients who arrived at the receiving center with inadequate blood pressure control. Air transport did allow coverage of areas more than twice the distance, but at eight times the cost. Important considerations that may change operative planning include the presence of connective tissue disorder and preexisting aneurysms in the aortic root or aortic arch. Dissections originating from preexisting aneurysms will likely require replacement of that segment. Degree of aortic valve regurgitation on preoperative echocardiography and any existing contraindications to anticoagulation will also have implications with regard to the need for aortic valve replacement and valve choice. Most surgeons perform proximal aortic dissection repairs during a period of hypothermic circulatory arrest.

For example acne essential oils buy cheap elimite on line, a 50% reduction in vessel radius causes a greater than 90% reduction in blood flow skin care 11 year olds 30gm elimite visa. Pressures are repeated approximately every 1 to 2 minutes until they return to baseline skin care logos elimite 30 gm sale. The time before ankle pressure returns to normal is increased in more severe disease acne in pregnancy order elimite 30gm line. Transcutaneous Oximetry By exploiting variations in color absorbance of oxygenated and deoxygenated hemoglobin (Hb) skin care jakarta selatan elimite 30 gm without a prescription, transcutaneous oximetry can determine the state of blood oxygenation acne medication oral cheap elimite 30 gm line. Oximeters use two light frequencies, red at 600 to 750 nm and infrared at 800 to 1050 nm, to differentiate oxygenated and deoxygenated Hb. Deoxygenated blood absorbs more red light, whereas oxygenated blood absorbs more infrared light. Red and infrared light is emitted and passes through a relatively translucent structure such as the finger or earlobe. A photodetector determines the ratio of red and infrared light received to derive blood oxygenation. When measured continuously, oxygenation peaks with each heartbeat as fresh oxygenated blood arrives in the zone of measurement. One probe is placed on the chest as a control to ensure that oxygen tension is from 50 to 75 mmHg. Measurements are obtained from the probe, which is sequentially positioned from proximal to distal segments of the limb. Because blood viscosity, blood vessel length, and pressure remain relatively stable, the most important determinant of blood flow is vessel lumen size. Vascular ultrasonography can depict flow velocity by taking advantage of Doppler shift frequencies. Frequency will shift either positively or negatively, depending on direction of blood flow. Variables that determine the size of the shift include the speed of sound, speed of the moving object, and angle between the 151 transmitted beam and moving object. Velocity is determined using the Doppler equation, with the cosine (cos) in the denominator. Tissue imaging enhancement may be noted on the far side of echofree or liquid-filled zones. Tissue interfaces may generate multiple sound wave reflections, causing "additions" to the tissue termed reverberation artifact. Refraction of the sound pulse may cause improper placement of a structure of an image and shadowing at the edge of a large structure. Highly reflective surfaces may create mirror images because the reflecting tissue alters the timing of the returning sound wave. High resistance Gray-Scale (B Mode) Imaging Ultrasound images are generated using a pulse echo system. The position of the tissue interface is determined by the time between pulse generation and returning echo. Each returning echo is displayed as a gray dot on a video screen using a brightness mode (B mode) in which the brightness of the dot depends on the strength of the reflected wave. A two-dimensional (2D) image is created by sequentially transmitting waves in multiple directions within a single plane and combining the reflected echoes in to a single display. The image can be refreshed rapidly, permitting realtime display of the gray-scale image. The surface of interest should be perpendicular to the ultrasound beam to obtain the brightest echo with B-mode imaging. This is readily achieved in vascular imaging because the neck, extremity, and visceral vessels generally lie parallel to the surface of the transducer. Higher-frequency probes are used to image vessels close to the surface, and lowerfrequency probes are used to image deeper vessels. The wide band width of transducers allows analysis of returning harmonics (whole-number multiples) of the fundamental frequency. These two waveforms are distinguished by the absence (high resistance) and presence (low resistance) of flow during diastole. Spectral Doppler Waveform Analysis Velocity recordings are obtained with an angle of 60 degrees between the Doppler insonation beam and the flow. In ultrasound practice, the optimal angle of measurement between the beam and blood flow is 60 degrees. Although maximal shift is detected at 0 degrees, this angle cannot be reliably obtained in vascular imaging because the vessels are parallel to the surface of the body. Insonation angles below and above 60 degrees influence the measurement such that small reductions in the insonation angle may alter velocity by 10%, whereas small increases in insonation angle may change flow velocity by 25%. Thus, the samplevolume cursor is placed parallel to the inner wall, and a Doppler9,10 angle from 30 to 60 degrees between the wall and the insonation beam (or flow jet) is used. A normal peripheral artery Doppler waveform consists of a narrow, sharply defined tracing. This indicates that all blood cells are moving at an equivalent speed at any time in the cardiac cycle. The first component is caused by initial high-velocity forward flow during ventricular systole. Flow is typically not uniform or laminar at bifurcations and sites of stenosis; at these sites flow becomes turbulent. For these locations, the spectral Doppler waveform reflects the fact that blood cells move with varying velocities. This third, or late, diastolic component is usually absent in atherosclerotic vessels that have lost compliance or elasticity. Color Doppler Color Doppler is the phase or frequency shift information contained in the returning echoes and processed in real time to form a velocity map over the entire imaging field. This information is then superimposed on the gray-scale image to provide a composite real-time display of both anatomy and flow. When motion is detected, it is assigned a color, typically red or blue, determined by whether the frequency shift is toward or away from the probe. Color assignment is arbitrary and can be altered by the user, but most choose to assign the color red to arteries and blue to veins. With increasing Doppler frequency shifts, the hue and intensity of the color display change, with progressive desaturation of the color and a shift toward white at the highest detectable velocities. Color persistence corresponds to the monophasic spectral Doppler waveform and is indicative of severe stenosis. This color artifact is associated with turbulence and occurs with flow disturbances associated with high-velocity jets. The pulse repetition frequency (velocity) scale determines the degree of color saturation and filling of the vessel lumen. The pulse repetition frequency (radio frequency pulses per second from the probe) is adjusted so that in a normal vessel, laminar flow appears as a homogeneous color. Increasing flow velocity and turbulence in the region of a stenosis results in production of a high-velocity jet and an abrupt change in color-flow pattern. Color aliasing occurs at the site of stenosis when flow velocity exceeds the Nyquist limit. Aliasing causes the color display to appear as if there is an abrupt reversal in direction of flow (wraparound). This suggests a high-velocity flow jet, requiring confirmation by pulsed-wave Doppler analysis. Color persistence is a continuous flow signal that is the color of the forward direction only, in contrast to the alternating color in normal arteries. Doppler velocity measurements are the main tools used to evaluate stenosis severity. When flow rate is constant, a decrease in vessel cross-sectional area is balanced by an increase in velocity. If no post-stenotic turbulence can be identified, inappropriate angle alignment or a tortuous vessel should be suspected. Power (or amplitude) Doppler is a complementary imaging technique that displays the total strength or amplitude of the returning Doppler signal. This enhanced dynamic range can depict very slow flow in the area of a subtotal occlusion that may not be detected by conventional color-flow Doppler. Contrast agents can also help differentiate between occlusion and highgrade stenosis in carotid and renal arteries, especially in cases where multiple renal arteries are present. The operator images the region from the clavicle to the angle of the jaw, in both anterolateral and posterolateral views. Carotid artery stenosis can be focal, and flow patterns can normalize within a short distance. Therefore, the pulse-wave sample volume should be methodically advanced along the length of the vessel; color Doppler may be used for guidance in delineating areas of abnormal flow requiring change in position of the sample volume. The vertebral artery is followed as far cephalad as possible, sampling the spectral Doppler in the accessible portions of the vertebral artery. There is an abrupt change from low-velocity laminar flow (A) to high-velocity flow with aliasing (B) as velocity exceeds Nyquist limits. This guides placement of spectral Doppler sample volume, identified by parallel white lines. A velocity waveform obtained from the proximal vessel or the site of maximal velocity should be obtained while intermittently tapping on the preauricular branch of the temporal artery. A number of criteria have been proposed, each having their own strengths and weaknesses (Table 12-1). At a minimum, velocity criteria must distinguish less than 50% stenosis, 50% to 69% stenosis, and greater than 70% stenosis. Selection of criteria for use in an individual laboratory requires review of the published parameters and selection of those appropriate to laboratory practice. Individual vascular laboratories must validate the results of their own criteria for stenosis against a suitable standard such as arteriography. Waveform evaluation is particularly valuable in the vertebral artery because the segments within the bone cannot be directly evaluated with ultrasound. Velocities greater than 125 cm/sec and dampened waveforms are two indicators of vertebral artery stenosis. Absent flow in the vertebral artery is confirmed when flow is detected in the vertebral vein, but not in the vertebral artery. Reverse flow is confirmed by comparing the direction of vertebral artery flow with that of the carotid artery. Reverse flow typically will have a diminished diastolic component because flow is in to the high-resistance bed of the subclavian artery. If flow is cephalad but notching is evident in the systolic portion of the wave, subclavian steal can be elicited by reexamining flow after arm exercise or following deflation of a blood pressure cuff that had been inflated to suprasystolic pressures on the ipsilateral arm. These maneuvers will increase demand in the subclavian bed, and vertebral flow will completely reverse in the setting of subclavian stenosis proximal to the vertebral origin. The probe is placed longitudinally above the clavicle and angled to obtain a scanning plane below the clavicle. Plaque and Arterial Wall Characterization Gray-scale imaging is used to evaluate carotid plaque and arterial wall characteristics. Echolucent plaque is characterized as plaque that is less echogenic than surrounding muscle. The volume of plaque is appreciated best in the transverse view and with three-dimensional (3D) reconstruction. Another potential technique to characterize plaque content and activity is contrast-enhanced ultrasound to detect ulceration and inflammation. Activated leukocytes attached to the inflamed vessel wall may bind the shells of lipid microbubbles, which are detectable by ultrasound. Plaque thickness can be severely overestimated or underestimated in the longitudinal image, and is best evaluated in transverse images. The flap may be apparent on gray-scale imaging but generally requires color or contrast for elucidation. A flutter is occasionally identified in the downslope of the waveform on the affected side. Evaluation should identify both the proximal and distal extent of dissection, and flow velocities in the true lumen. Carotid Intima Media Thickness Carotid ultrasonography has traditionally been used to evaluate the presence of obstructive atherosclerosis in the setting of symptomatic cerebrovascular disease or asymptomatic carotid bruit. Intima media thickness measurement is most commonly made from longitudinal images, with the assistance of semiautomated edge-detection software. There is variability in this measurement from systole to diastole, and by age and gender. Wall thickening is evident between intima lumen interface (a) and media adventitia interface (b). Distance between intima lumen border and media adventitia border is determined with automated edge-detection program that averages thickness of wall over region, identified by blue lines laid over these borders. Abdominal Aorta Evaluation Abdominal ultrasound is used to diagnose and follow abdominal aortic aneurysms. The patient is required to fast prior to the study because bowel gas will obscure imaging. Aortic ultrasound scanning begins with the patient supine and the transducer placed in a subxiphoid position.

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This plateau reflects dissipation of energy across the stenotic lesions skin care quotes discount elimite 30gm overnight delivery, removing any additional driving force for increase in flow acne denim buy elimite visa. Despite the plateau in oxygen delivery during exercise skin care lotion order elimite 30gm line, further increases in oxidative work output are supported by increases in muscle oxygen extraction delex acne elimite 30gm on line. The resultant mismatch between the demands for bioenergetics and the flow supply also contribute skin care routine for oily skin generic elimite 30 gm free shipping. Critical Artery Stenosis the hemodynamic significance of an arterial stenosis is not only a function of the percent stenosis acne oral medication buy elimite 30gm with visa, but also linear flow velocity across the lesion, as reflected in the Poiseuille equation. The concept integrates the relationship of a stenotic narrowing in an artery with arterial flow velocity and the resultant volumetric flow distal to the stenosis. Importantly, a critical artery stenosis may differ between resting and exercising states because flow velocity in these two conditions is different. Because the pressure gradient across any given stenosis is proportional to the flow velocity, states of higher flow velocity, as occurs with exercise, may result in a decrease in distal perfusion pressure, whereas states of lower velocity, as occurs at rest, may not. For example, resting blood flow velocity in the femoral artery may be only 10 to 20 cm/s, corresponding to a downstream calf blood flow of 1 to 2 mL/100 mL of tissue/min. Distal flow will be maintained, since the mild reduction in perfusion pressure will be compensated by a reduction in downstream peripheral resistance. Once the stenosis becomes greater than 90%, there is a greater pressure gradient and fall in distal perfusion pressure, and changes in peripheral resistance can no longer compensate. In this example, the critical arterial stenosis needed to reduce distal blood flow at rest is 90%. Other Contributors to Altered Blood Flow in Peripheral Artery Disease Although arterial flow limitations are of critical importance in the pathophysiology of claudication, the hemodynamic status of the limb correlates poorly with exercise performance. After exercise-induced claudication, total neutrophil number and the proportion of activated neutrophils are higher in venous blood draining from the affected leg than in arterial blood. Furthermore, activated leukocytes release thromboxane A2 (TxA2), which is a vasoconstrictor and promotes platelet aggregation. Thus the generation of free radicals and oxidative stress can be mediators of tissue injury. Leukocytes may play an important role in ischemic disease via formation of microemboli and induction of oxidative damage. Activated neutrophils may adhere to other leukocytes and blood cells, further narrowing the vessel lumen and, through release of mediators, increasing vessel wall damage. In one study, P-selectin expression was significantly increased in patients with intermittent claudication and critical ischemia compared to controls. Sequelae are increase in expression of mitochondrial enzymes and accumulation of lactate and acylcarnitines. Kreb Cycle Increased Expression Mitochondrial Enzyme Glucose Fatty Acids Lactate Accumulation Acylcarnitine Accumulation. These steps have been previously identified as targets of oxidative injury in myocardial perfusion-reperfusion models. Supplementation with the antioxidant vitamin C improves endothelial function in patients with diabetes. Muscle Structure and Function in Peripheral Artery Disease In healthy humans, exercise requires coordinated recruitment of appropriate muscle fiber types to meet the demands of specific exercise conditions. There is recruitment of type I oxidative slowtwitch fibers that have high mitochondrial content with low-intensity repetitive contractions. Depending on the exercise intensity of these contractions, the fuel is a balance of fat and carbohydrate oxidation. These fibers have fewer mitochondria than type I fibers and have easy fatigability. These changes reflect a complex combination of changes associated with disuse due to exercise limitation and direct injury from ischemia, ischemia-reperfusion, and chronic inflammatory mechanisms. Patients with claudication also demonstrate extensive skeletal muscle denervation by histological criteria. Denervation injury has been confirmed by electrophysiological testing, and these abnormalities are progressive over time. The neurophysiological changes suggest that the underlying pathophysiology is a distal axonopathy affecting nerve fibers of all sizes. Measures of blood flow in the leg correlate with neurological symptom scores, examination scores, and electrophysiological testing. Increased capillarity may be in compensation for the reduction in large-vessel blood flow, and these changes in peripheral diffusion (higher conductance) may have functional relevance. Whether these gait abnormalities are related to muscle denervation and weakness or are adaptations to minimize development of pain is unknown. Muscle mitochondrial content and mitochondrial enzyme activities reflect the functional state of the individual. Skeletal muscle mitochondrial oxidative enzyme activities increase with exercise training and decrease with prolonged bed rest or inactivity. An increased mitochondrial content might improve oxygen extraction under ischemic conditions and could reflect a compensatory mechanism for any intrinsic abnormality in mitochondrial oxidative capacity. During normal metabolic conditions, fuel substrates such as fatty acids, protein, and carbohydrates are converted to acyl-coenzyme A (CoA) intermediates for oxidative metabolism in the Krebs cycle. Thus, during conditions of metabolic stress, incomplete oxidation or utilization of an acyl-CoA will lead to their accumulation. Transfer of the acyl group to carnitine will result in accumulation of the corresponding acylcarnitine. Importantly, acylcarnitine accumulation may have functional significance in that patients with the greatest accumulation have the most reduced treadmill exercise performance. This limitation in the blood flow response to exercise has metabolic consequences. At the onset of exercise, however, there is a marked delay in systemic uptake of oxygen that parallels a slowed response in skeletal muscle uptake of oxygen. Large-vessel obstruction impairs delivery of oxygenated blood to skeletal muscle during exercise, resulting in a supply/demand mismatch. Arterial hemodynamics and large-vessel blood flow, however, do not fully account for the exercise limitations observed in patients with claudication. Understanding these multiple components of exercise limitation provides insight in to treatment approaches that address the spectrum of abnormalities seen in patients with claudication. Critical limb ischemia is a state characterized by severe impairment of blood flow to the limb whereby the metabolic requirements of the tissue at rest are not met. Multiple occlusive lesions of the limb arteries, coupled with functional and structural changes in the microcirculation, are responsible for inadequate tissue perfusion and formation of skin ulcers and necrosis. Blood components such as red cells, white cells, and platelets aggregate and perturb blood flow in the microcirculation. Dormandy J, Mahir M, Ascady G, et al: Fate of the patient with chronic leg ischaemia. Ciuffetti G, Mercuri M, Mannarino E, et al: Free radical production in peripheral vascular disease. Jansson E, Johansson J, Sylven C, et al: Calf muscle adaptation in intermittent claudication. Creager activity cessation rebalances available blood supply with muscle demand and quickly resolves the pain. Both time of activity to pain onset and time to pain resolution should be consistent and predictable. The distance walked to the onset of leg discomfort is called the initial claudication distance, and the maximal distance the patient can walk without stopping because of leg discomfort is called the absolute claudication distance. Several classification schemes are used to categorize the severity of claudication, including the Fontaine (Table 18-1) and Rutherford classifications (Table 18-2). Patients with pain at rest and with walking had worse functional capacity than those whose pain occurred with walking and stopped with walking cessation, and those who were able to "walk through" the pain. Three quarters of patients with intermittent claudication will have stable symptoms over the next 10 years; approximately 25% will progress to more disabling claudication or critical limb ischemia requiring revascularization or culminating in amputation. This chapter will focus on the history, physical examination, and diagnostic tests important to management of limb atherosclerosis. This includes avid questioning and seeking to elicit historical evidence of limb and systemic atherosclerosis. Clinical suspicion should be heightened in older persons, in those with coronary or cerebral atherosclerosis, and in patients with atherosclerotic risk factors such as diabetes or tobacco use, as well as renal failure (see Chapter 16). Thus, the presence of risk factors for atherosclerosis should lower the threshold for routine screening. Differential Diagnosis of Claudication Once exercise-related discomfort has been established, several alternate vascular and nonvascular diagnoses should be considered (Box 18-1). Vascular disorders include popliteal artery entrapment (see Chapter 62), compartment syndrome, fibromuscular dysplasia, venous insufficiency (see Chapter 55), and vasculitis (see Chapters 41 through 45). Because of an abnormal origin of the medial (or less commonly, lateral) head of the gastrocnemius muscle, the popliteal artery may be compressed with walking and yield symptoms of claudication. Fibromuscular dysplasia is a noninflammatory arterial occlusive disease that most commonly affects the renal and carotid arteries but may involve other arterial beds (see Chapter 63). The word claudication derives from the Latin word claudicatio, which was used to describe the limp gait of a lame horse. As defined in the Rose questionnaire,6 claudication is development of an ischemic muscular pain on exertion. The pain can be characterized as aching, burning, heaviness, feeling leaden, tightness, or cramping. Pain should originate in a muscular bed, such as the calf, thigh, hip, or buttock, and not localize to a joint. The area of the worst blood flow limitation usually subtends the site of muscular discomfort. For example, patients who develop hip or buttock discomfort with walking most likely have distal aorta or iliac artery occlusive disease, whereas patients with calf claudication likely have superficial femoral or popliteal arterial stenoses or occlusions. Patients may complain of leg pain or paresthesias as a result of compression of the lumbar nerve roots from disc herniation or degenerative osteophytes. The paresthesias or pain tend to affect the posterior aspect of the leg and occur with specific positions such as standing or develop at the beginning of ambulation. These symptoms may improve with continued walking or when leaning forward because pressure on the nerve roots is reduced. The pain may be confused with intermittent claudication because it typically occurs with exercise. It can be distinguished from claudication in that the level of activity required to precipitate symptoms varies and does not resolve rapidly with activity cessation. Diabetes is the cause of most nontraumatic lower-extremity amputations in the United States. The pain is often severe and unremitting and localized to the acral portion of the foot or toes, notably at the site of ulceration or gangrene. Blood flow limitation is so severe that the gravitational effects of leg position may affect symptoms. This is typically worse at night when the patient is in bed and the leg, now at heart level, no longer benefits from the dependent position. Placing the foot on the floor beside the bed is a common action used by patients to reduce pain. Inability to use the leg and chronically placing the leg in a dependent position may cause Box 18-1 Nonatherosclerotic Causes of Exertional Leg Pain Nonatherosclerotic arterial disease Atheroembolism Vasculitis Extravascular compression Popliteal artery entrapment Adventitial cysts Fibromuscular dysplasia Endofibrosis of the internal iliac artery Venous claudication Compartment syndrome Lumbar radiculopathy Spinal stenosis Hip/knee arthritis Myositis arteries in the lower extremities may be affected, but the iliac arteries are the most common. It can be diagnosed from the "string of beads" appearance on angiography and by its predilection for the nonbranching points of vessels.