Peripheral Arterial Disease (PAD) - Essay Example

Peripheral Arterial Disease (PAD) Introduction Peripheral arterial disease (PAD) is a chronic arterial occlusive disease of the lower extremities as result of atherosclerosis. Computed tomography angiography (CTA) produces detailed images of blood vessels and tissues of the extremities, and is thus, helpful in the diagnosis of PAD. Earlier, CTA technology was able to image only a portion of the peripheral arterial tree. Later, the multi-detector row CT (MDCT) technology evolved. In 1998, with the arrival of four-detector row CT (4D-CT), a complete coverage of the lower extremity inflow and runoff arteries with one acquisition using a single-contrast bolus, was possible. Further, with the 16-detector row CT (16D-CT), the spatial resolution increased and the contrast medium efficiency improved. Finally, with the 64-detector row CT (64D-CT) scanner, a true isotropic high spatial resolution of the entire volume was possible. Thus, the multi-detector row CT angiography (MDCTA) has developed as an accurate method in assessing the peripheral arteries. Clinical history Some of the risk factors for PAD include cigarette smoking, increased plasma homocysteine levels, hypothyroidism, diabetes mellitus, and hypertension (Aronow, 2007). Rare causes are hypercoagulable states, such as protein C or S deficiency or antithrombin III deficiency, and the vasospastic syndromes (Garcia 2006.)    One of the main symptoms in a person with PAD is intermittent claudication, “which is pain or weakness with walking that is relieved with rest” (Aronow 2007). This occurs distal to where the artery is obstructed. Most commonly, atherosclerosis affects the superficial femoral and popliteal arteries, and thus, the pain is most often in the calf muscle. In case the atherosclerotic obstruction is at the distal aorta and its bifurcation into the two iliac arteries, the pain may be felt, in addition to the calf, in the buttocks, hips, thighs, or the inferior back muscles (Aronow 2007) “The Rutherford classification of PAD includes 7 stages. PAD is classified as stage 0 if the person is asymptomatic, stage 1 if mild intermittent claudication is present, stage 2 if moderate intermittent claudication is present, stage 3 if severe intermittent claudication is present, stage 4 if ischemic rest pain is present, stage 5 if the person has minor tissue loss, and stage 6 if the person has ulceration or gangrene” (Aronow 2007.) If PAD involves the upper extremities, then the blood pressure measurements in each arm will be unequal. There is also a higher prevalence of cognitive impairment and erectile dysfunction in patients with PAD. Critical lower extremity ischemia can occur whenever the arterial blood flow to the lower extremities is not sufficient to meet the requirements of resting tissue metabolism. As a result of this, pain in the toes or foot can occur even with rest and this can progress to ulceration or gangrene (Aronow 2007). Ulceration commonly develops at the leg, ankle or heel. Ischemic infarction causes gangrene, which appears as “mummified, dry, black toes or devitalized soft tissue covered by a crust” (Aronow 2007). Over a period of time, suppuration develops and dry gangrene changes to wet gangrene. Physical examination of the vascular system includes: blood pressure measurement in both arms, carotid pulse palpation and auscultation for bruits, abdominal and flank auscultation for bruits, palpating pulses at brachial, radial, ulnar, femoral, popliteal, dorsalis pedis, and posterior tibial sites, and auscultating both femoral arteries for femoral bruits. Feet should be inspected for color, temperature, and integrity of the skin, distal hair loss, trophic skin changes, hypertrophic nails, and ulcerations (Aronow 2007). Pathology Atherosclerosis, which primarily is a systemic inflammatory process, is the most common cause of PAD. Histopathologically, an atherosclerotic lesion is initiated with the appearance of fatty streaks, which initiates an inflammatory process. This promotes the deposition of cholesterol, and finally, plaque buildup (Garcia 2006). Plaque is made up of fat, fibrin, cellular waste products, cholesterol and calcium.  Over a period of time, the wall of the artery becomes thickened and becomes inelastic (Garcia 2006). As a consequence of the plaque buildup, the amount of blood flow to the limbs is reduced, which in turn decreases the nutrients and oxygen required by the tissues. Clots, which may develop on the arterial wall, further decreases the inner lumen size, and thus can block the artery (University of Virginia 2010). This atherosclerotic lesion might either remain stable, or it can develop a thin, unstable fibrous cap, which can ulcerate. Once ulceration develops, the underlying plaque gets exposed to the bloodstream, and cause a thrombotic occlusion or embolization (Garcia 2006.) Patient preparation for CT angiography for PAD The patient is asked to lie in the supine position on the CT table with the arms raised, and without any movement (Kock et al 2007). The patient’s knees and feet are carefully aligned and positioned close to the gantry isocenter (Kalra 2006). Cushions, which are placed around the legs and strapped with adhesive tape distally, help to stabilize the legs. The patient is checked whether their clothing contains any metal zippers or buttons because this can impair the quality of the image (Kock et al 2007). “The anatomical scan length for a typical lower-extremity CTA study is 110-130 cm and extends from the renal artery origins at T12 vertebra to the patient’s feet” (Kalra 2006.) Scanning protocol It is possible to program the complete protocol into the scanner. By using a scanogram of approximately 1,500-mm length, it is possible to plan the acquisition coverage from the celiac trunk (T12 vertebral body) to the level of the talus (using 4D-CT) or to the level of the feet (using 16D-CT or higher) (Kock et al 2007). For an average sized patient, 120 kV and 300 mA is used. For smaller patients a lower tube current and/or tube potential can be used, while for obese patients a greater current and potential can be used (Kalra 2006.) Depending on the number of detector rows and the collimation, the optimal scan duration for peripheral CTA is around 20 to 40 s. In PAD, the average velocity of travel of a contrast bolus (from the aorta to the popliteal arteries) is 29 to 177 mm/s. Therefore, it is recommended that the maximum table speed be limited to 30 mm/s on faster scanners. This helps to avoid outrunning the bolus, which can lead to poor distal vessel opacification. The maximum table speed can be limited by limiting the speed of the gantry rotation from 0.33 to 0.5 rotations per second or reducing the pitch. It is also recommended that a second acquisition protocol be programmed into the scanner, which will start if a delayed distal enhancement is detected. A scan duration longer than 7 to 40 s can increase the risk of venous contamination (Kock et al 2007). With the latest MDCT scanners, fast scans (25 s or less) can be done, which helps to reduce the amount of contrast media used (Kock et al 2007). By using a thin section collimation width, it is possible to get a maximal spatial resolution, as well as reduce the partial volume effect and blooming effect of calcium (Kock et al 2007) Contrast protocol Generally, about 1-1.5 g of iodine/second is injected intravenously into the antecubital vein using 20 and 22-gauge cannulas. This gives a maximal flow rate of 3.5 and 5.0 mL/s. For heavier or lighter patients, a patient –weight-based adjustment of contrast volume and flow rate is made (Kalra 2006). By ensuring that the injection duration is not shorter than 30 seconds, enhancement of all arteries is possible. In case of fast scan protocols, an adequate delay time has to be added. This prevents outrunning the contrast bolus. A flow rate of 3 to 4 ml/s is necessary for adequate arterial enhancement. Oral contrast is not used, since it can complicate postprocessing display. In order to decrease the viscosity, the contrast material is injected at body temperature. A monophasic injection rate is used in clinical practice since it is simple and results in an adequate image quality (Kock et al 2007). Attenuation values higher than 200 HU in the arteries is generally thought to be adequate in (Kock et al 2007). “By increasing the iodine concentration to a concentration of 400 mg I /mL, the iodine administration rate can be increased to 1.6 g/s to increase the enhancement. To optimize the enhancement, 20 to 60 mL of saline is injected immediately after the contrast media. A tighter bolus can be obtained to increase the attenuation” (Kock et al 2007). Several timing techniques are used like the test-bolus technique, and the bolus-triggering technique (Kock et al 2007). Strategies to reduce radiation dose With MDCT scanners there is a potential to deliver higher radiation doses. In order to address this issue, most current MDCT scanner consoles indicate the dose delivered to a patient; this also optimizes the scan protocol. It is also possible to achieve dose reduction by using automatic tube current modulation, which decreases the tube current. Unnecessary x-rays in the anterior–posterior projection can be reduced by using angular tube current modulation, which changes the attenuation through different projections around the patient. Longitudinal tube current modulation a dose reduction of 20% or more can be obtained. It has, however, been estimated that the average patient dose with CTA in PAD is 7.47 mSv, which is not very worrying (Kock et al 2007). Image display, appearance and analysis (2D/3D reconstruction) Over 1,500 axial images are generated by peripheral CTA. Therefore, it is recommended that separate data sets be reconstructed. An increment with 50% to 70% overlap is used to reconstruct the raw data set. Usually, three separate data sets of the peripheral runoff are calculated. Generally, in CTA, a smooth kernel is used, which accurately depicts vessel diameter, and is ideal for postprocessing. Whenever stents or severe vessel wall calcifications are present, a sharp kernel is used. In order to optimize the pixel size, as small as possible field of view (FOV) is selected (Kock et al 2007). In order to facilitate interpretation and presentation, additional two-dimensional (2D) and three-dimensional (3D) postprocessing techniques are needed (Kock et al 2007). Cross-sectional (2D) detail allows detailed analysis of flow channel and vessel wall. The techniques include multiplanar reformations (MPR) and curved planar reformation (CPR). The advantages are that allows accurate grading of stenosis/occlusion, even in the presence of calcification and stents. However, the limitation is limited spatial perception. Volumetric (3D) overview provides a general overview of vessel tree, including collaterals. The techniques include maximum intensity projection (MIP) and volume rendering (VR). The advantages are excellent spatial perception and easy display of findings to referring physician. The limitations include obscuration of portions of vessel tree and obscuration of vessel lumen in the presence of stents and calcified plaque (Catalano and Passariello 2005.) There are a set of standard postprocessed images, which are included in the protocol. These include thin-slab maximum-intensity projections (MIPs) (through visceral and renal arteries, abdominal aorta, femoropopliteal arteries, and crural arteries); curved planar reformations (CPRs), whole-volume MIPs and Volume-rendered (VR) images. Vessel lumen visibility can decrease if extensive calcifications or stents are present. Superimposing calcifications in whole-volume MIPs can selectively be removed digitally. In extensively calcified arteries, CPR is a good technique for stenosis detection (Kock et al 2007). Wall calcifications are present in approximately 20% to 50% of the vascular segments, which can impair lumen assessment. A better differentiation of calcifications and stents from the enhanced lumen can be obtained by using a wider window width (WW) and higher window center (WC) level settings. In case of circumferential calcifications, transverse images, CPR images, and the digital removal of the calcifications can help (Kock et al 2007). After care of patients About 2-6 hours of supervised recovery is normal. Too much physical activity is avoided. Normal activities can be resumed the next day. A good fluid intake is recommended. Apart from any other medication that the patient has been taking, painkillers can be taken for any pain. In case there is any bleeding at the site where the catheter was inserted, the patient is asked to put direct pressure to the bleeding and return to the hospital. The patient is also asked to return if their foot gets cold, numb, or painful (Saskatoon Health Region.) Treatment and prognosis 1. Medical treatment a. Antiplatelet drugs-specifically, aspirin (75-325 mg/day) and /or clopidogrel (75mg/day). b. Risk-factor modification-smoking cessation, strict control of sugar levels (if diabetic), blood pressure control, lipid modification and supervised exercise rehabilitation (Jaff 2008.) Six products have been approved by the FDA for smoking cessation: sustained-release bupropion and five nicotine-replacement products (i.e., transdermal patch, nicotine gum, lozenge, a vapor inhaler and a nasal spray). The use of such nicotine-replacement products helps to increase the rates of smoking cessation by the patient in the long-term, as well as reduce nicotine cravings and the symptoms of nicotine withdrawal. The benefits of lipid-lowering therapy have been demonstrated in many large scale clinical trials in patients with PAD. Initial therapy is started with a statin drug. Niacin is also considered because it is known to increase serum high-density lipoprotein (HDL) concentrations, while lowering the serum triglyceride levels (Gey, Lesho and Manngold 2004)   Even though serum homocysteine levels are known to reduce by diet supplementation with vitamin B and folate, there are no controlled trials, which show that a reduction in the levels of serum homocysteine would benefit patients with PAD. Perhaps the most effective treatment of PAD is a formal exercise program. More than 20 controlled trials have demonstrated its effectiveness (Gey, Lesho and Manngold 2004)   c. Cilostazol- four trials have shown that cilostazol, which is an inhibitor of phosphodiesterase type 3, has been shown to significantly improve walking distance by 20%–40% (Norman, Eikelboom and Hankey 2004.) d. Anticoagulants and calcium channel blockers to reduce hypertension e. Foot care 2. Surgical treatment a. Angioplasty and stenting-angioplasty involves the insertion of a long, thin, flexible catheter through a small puncture over an artery in the arm or groin. It is passed through the arteries to the blocked area, where a balloon attached to the catheter is inflated and deflated, repeatedly. This widens the artery. At times a stent may be placed in this area (Vascular Web 2010.) b. Bypass surgery-this involves creating a bypass around the narrowed, or blocked, section of a leg artery by using the patient’s own vein or a synthetic tube. This is required for extensive blockages of the artery (Vascular Web 2010.) c. Endarterectomy-this involves making an incision and removing the plaque in the involved artery (Vascular Web 2010.) d. Amputation-this is a last resort method for gangrenous legs. Amputation of the lower leg or foot is done (Vascular Web 2010.) Prognosis Few patients with intermittent claudication have worsening leg symptoms like rest pain, ischemic ulceration or gangrene. About 10%–20% of patients with intermittent claudication require intervention like angioplasty or bypass surgery (Norman, Eikelboom and Hankey, 2004.) About 1%–2% of patients require amputation. Continued smoking, diabetes and a low initial ABPI are the main risk factors for amputation. There is a 4%–6% risk of cardiovascular death in patients with PAD.  Those patients with symptomatic PAD have a 15-year accrued survival rate of about 22%, while patients without symptoms of PAD have a survival rate of 78%. Those patients with critical leg ischemia have an annual mortality of 25% (Norman, Eikelboom, Hankey and 2004.) Conclusion Peripheral arterial disease (PAD) is a chronic arterial occlusive disease of the lower extremities as result of atherosclerosis. One of the main symptoms in a person with PAD is intermittent claudication. Most commonly, atherosclerosis affects the superficial femoral and popliteal arteries, and thus, the pain is most often in the calf muscle. Critical lower extremity ischemia can result in pain in the toes or foot even with rest and this can progress to ulceration or gangrene. Multi-detector row CT angiography (MDCTA) has established itself as a reliable and accurate method of diagnosing PAD. The optimal scan duration for peripheral CTA is around 20 to 40 s. Iodine is used for contrast. A flow rate of 3 to 4 ml/s is necessary for adequate arterial enhancement. Automatic tube current modulation, angular tube current modulation and longitudinal tube current modulation are some methods to reduce radiation dose. In order to facilitate interpretation and presentation, additional two-dimensional (2D) and three-dimensional (3D) postprocessing techniques are needed. The patient can return to routine activities the next day after the CTA, and is advised not to strain and report if there are any problems like bleeding. The treatment of PAD includes medical (antiplatelets, cilostazol, risk-factor modification, and foot care) and surgical (angioplasty and stenting, bypass surgery, endarterectomy and amputation). In general, the prognosis for PAD is good, provided that the patient does not have risk factors like diabetes or continued smoking. CT images of PAD Peripheral multi–detector row CT angiogram in a patient with Leriche syndrome. This coronal volume maximum intensity projection shows a complete occlusion of the abdominal aorta and both iliac arteries and indicates that there is collateral arterial supply from enlarged epigastric arteries in the abdominal wall (arrowheads), superficial iliac circumflex arteries (straight arrows), and a superficial external pudendal artery (curved arrow) (From Radiology November 2005 vol. 237 no. 2 727-737) Fig 2. Data trimming MIP image demonstrating the popliteal artery block with distal reformation (from Indian Journal of Radiology and Imaging) Fig3. Coronal, sagittal and data trimmed MIP images of a patient of PVD showing the near complete stenosis (grade III) of the right SFA with good distal reformation through the collaterals and narrowing (grade II) of the left SFA (from Indian Journal of Radiology and Imaging) References Aronow, WS. “Peripheral arterial disease in the elderly.” Clin Interv Aging (2007). 2(4): 645–654. Catalano, C and Passariello, R. Multidetector-row CT angiography. Springer, 2005. Garcia, LA. “Epidemiology and Pathophysiology of Lower Extremity Peripheral Arterial Disease.” Journal of Endovascular Therapy (2006). 13: II-3-II-9. Gey, Lesho and Manngold, 2004. “Management of Peripheral Arterial Disease.” http://www.aafp.org/afp/2004/0201/p525.html (accessed April 7, 2010). Jaff, MR. Peripheral arterial disease. McNaughton & Gunn, 2008.    Kalra, MK. Mdct: From Protocols to Practice. Springer, 2006. Kock, MCJM, Dijkshoorn, ML, Pattynama, PMT, Hunink, MGM. “Multi-detector row computed tomography angiography of peripheral arterial disease.” Eur Radiol. (2007). 17(12): 3208–3222. Norman, PE, Eikelboom, JW, Hankey, GJ. “Peripheral arterial disease: prognostic significance and prevention of atherothrombotic complications.” MJA.  (2004). 181 (3): 150-154. Saskatoon Health Region. “Tests & Procedures Angiography - Guidelines for Patients Post-Procedure Guidelines.” http://www.saskatoonhealthregion.ca/your_health/tp_angio_post_angio.htm (accessed April 7, 2010). University of Virginia, 2010. “Peripheral Vascular Disease (PVD).” http://www.healthsystem.virginia.edu/UVAHealth/adult_cardiac/peripher.cfm (accessed April 7, 2010). Vascular Web, 2010. “Peripheral Artery Disease.” http://www.vascularweb.org/patients/NorthPoint/Leg_Artery_Disease.html (accessed April 7, 2010). Read More